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We aimed to investigate the expression of cancer susceptibility candidate 11 (CASC11) in ovarian cancer (OC) tissues and its role in doxorubicin (Dox) resistance. A total of 98 patients were included as subjects. Reverse transcription-polymerase chain reaction was employed to determine the expressions of CASC11 in OC and para-OC tissues, and in OC cells (A2780, SKOV3, OVCAR3 and A547) and human normal ovarian epithelial cells (IOSE-80) from these patients. OC SKOV3/R cell line with Dox resistance was established and transfected with small interfering (si)-CASC11 to down-regulate CASC11 expression. Based on the constructed nude mouse model of orthotopic transplanted tumor, the growth curves were plotted, and the changes in tumor volume and apoptosis were observed by hematoxylin-eosin staining. OC tissues had a significantly higher mRNA expression of CASC11 than that of para-OC tissues (P < 0.05). A547, OVCAR3, A2780 and SKOV3 cells had significantly higher mRNA expressions of CASC11 than that of IOSE-80 cells (P < 0.05). The transplanted tumor was significantly smaller in volume in the si-CASC11 group than that in the si-normal control (NC) group from the 8th days after transplanted tumor inoculation (P < 0.05). The tumor growth inhibition rate significantly rose in the si-CASC11 group in comparison with that in the si-NC group (P < 0.05). CASC11 has high expression in OC tissues. Knockout of CASC11 weakens the proliferative, invasive and migratory potentials and enhances the apoptotic potential of Dox-resistant OC cells, thereby reversing their Dox resistance.
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Perineural invasion (PNI) is a notorious feature of salivary adenoid cystic carcinoma (SACC) and other neurotropic tumors. The pathogenesis of PNI that involves the molecular communication between the tumor and the suffered nerve is elusive. The in vitro co-culture assays of SACC cells with dorsal root ganglia (DRG) or neural cells showed that nerve-derived CCL2 activated CCR2 expression in SACC cells, promoting the proliferation, adhesion, migration, and invasion of SACC cells via the ERK1/2/ITGß5 pathway. Meanwhile, SACC-derived exosomes delivered ITGß5 to promote the neurite outgrowth of neural cells or DRG. Blocking of CCL2/CCR2 axis or ITGß5 inhibited the PNI of SACC cells in models in vitro by 3D co-culture of DRG with SACC cells and in vivo by xenografting SACC cells onto the murine sciatic nerve. High levels of ITGß5 in tissues or plasma exosomes were significantly correlated with CCL2 and CCR2 expression in the tissues and associated with PNI and poor prognosis of SACC cases. Our findings revealed a novel reciprocal loop between neural and tumor cells driven by the CCL2/CCR2 axis and exosomal ITGß5 during PNI of SACC. The present study may provide a prospective diagnostic and anti-PNI treatment strategy for SACC patients via targeting the nerve-tumor interactions.
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OBJECTIVES: To assess the prognostic significance of extra-pancreatic organ invasion in patients with resectable pancreatic ductal adenocarcinoma (PDAC) in the pancreas tail. MATERIALS & METHODS: This retrospective study included patients with resectable PDAC in the pancreas tail who received upfront surgery between 2014 and 2020 at a tertiary institution. Preoperative pancreas protocol computed tomography (CT) scans evaluated tumor size, peripancreatic tumor infiltration, suspicious metastatic lymph nodes, and extra-pancreatic organ invasion. The influence of extra-pancreatic organ invasion, detected by CT or postoperative pathology, on pathologic resection margin status was evaluated using logistic regression. The impact on recurrence-free survival (RFS) was analyzed using multivariable Cox proportional hazard models (clinical-CT and clinical-pathologic). RESULTS: The study included 158 patients (mean age, 65 years ± 8.8 standard deviation; 93 men). Extra-pancreatic organ invasion identified by either CT (p = 0.92) or pathology (p = 0.99) was not associated with a positive resection margin. Neither CT (p = 0.42) nor pathological (p = 0.64) extra-pancreatic organ invasion independently correlated with RFS. Independent predictors for RFS included suspicious metastatic lymph node (hazard ratio [HR], 2.05; 95 % confidence interval [CI], 1.08-3.9; p = 0.03) on CT in the clinical-CT model, pathological T stage (HR, 2.97; 95 % confidence interval [CI], 1.39-6.35; p = 0.005 for T2 and HR, 3.78; 95 % CI, 1.64-8.76; p = 0.002 for T3) and adjuvant therapy (HR, 0.62; 95 % confidence interval [CI], 0.42-0.92; p = 0.02) in the clinical-pathologic model. CONCLUSION: Extra-pancreatic organ invasion does not independently influence pathologic resection margin status and RFS in patients with resectable PDAC in the pancreas tail after curative-intent resection; therefore, it should not be considered a high-risk factor.
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BACKGROUND: Laryngocarcinoma is a common malignancy in the upper respiratory tract. Enabled homolog (ENAH) is an actin-binding protein that is associated with the development of various cancers. However, its role and mechanism in laryngocarcinoma remain unknown. METHODS: The ENAH level in laryngocarcinoma was examined in silico, in vitro and in vivo. The prognostic analysis of the ENAH level was assessed on laryngocarcinoma patients. Gain- and loss-of-function assays were conducted in AMC-HN-8 and TU686 cells. Sh-ENAH-containing AMC-HN-8 cells were implanted into naked mice. The role and mechanism of ENAH in laryngocarcinoma were investigated by CCK-8, transwell, immunofluorescence, dual luciferase, RT-qPCR, immunohistochemistry, and western blotting experiments. RESULTS: The ENAH level was upregulated in laryngocarcinoma, which predicted a poor prognosis in laryngocarcinoma patients. Gain- and loss-of-function results showed that ENAH promoted proliferation, invasion and EMT of laryngocarcinoma cells. Moreover, ENAH was transcriptionally activated by YY1, and YY1/ENAH axis enhanced these malignant progresses of laryngocarcinoma cells. Besides, ENAH activated the PI3K/AKT pathway, and 740Y-P abolished the accelerative role of ENAH in proliferation, invasion and EMT of laryngocarcinoma cells. Furthermore, knockdown of ENAH reduced tumor size and weight, and the expression level of vimentin and PI3K/AKT pathway in tumor-bearing mice. CONCLUSION: ENAH transcriptionally activated by YY1 promotes cell growth, invasion and EMT of laryngocarcinoma through the activation of PI3K/AKT signaling.
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The malignant behavior and immune escape ability of cancer cells lead to therapeutic failure and poor prognosis for patients with various cancers, including colon cancer. Plexin domain containing 1 (PLXDC1) was initially identified to exert key roles in tumor by regulating angiogenesis and has recently proved to be involved in cell proliferation and migration of glioblastoma and gastric cancer cells. However, its roles in colon cancer remain unclear. In this study, the online bioinformatics databases confirmed high expression of PLXDC1 in colon cancer specimens, which was associated with cancer stages and nodal metastasis. Similarly, the increased expression of PLXDC1 was also validated in our collected samples and colon cancer cells. Moreover, patients with high expression of PLXDC1 had shorter survival, indicating that PLXDC1 might be a potential prognostic predictor for colon cancer patients. Notably, targeting PLXDC1 inhibited cancer cell viability and invasion, and enhanced cell apoptosis. Intriguingly, Tumor Immune Estimation Resource database confirmed that PLXDC1 expression was related to various tumor-infiltrating immune cells in colon adenocarcinoma including macrophages, and its expression was also correlated with M2-like macrophage markers. In vitro, colon cancer cells with PLXDC1 downregulation had a reduced ability to recruit and polarize macrophage towards M2 phenotype by decreasing the percentage of CD206+ cells and M2-like markers (CD206, CD163, arginase1, and interleukin 10 [IL-10]). Moreover, PLXDC1 knockdown attenuated M2 macrophage-mediated promotion in cancer cell viability and invasion. Mechanically, inhibition of PLXDC1 suppressed activation of the IL-6/Signal transducer and activator of transcription 3 (STAT3) signaling. Reactivating the above pathway by transfection with IL-6 plasmids reversed the suppressive effects of PLXDC1 knockdown on cancer cell malignant behaviors, macrophage recruitment and M2-like polarization. Thus, PLXDC1 downregulation may inhibit the malignancy of colon cancer cells and their ability to recruit and polarize macrophages towards M2 phenotype by blocking the IL-6/STAT3 pathway. Together, targeting PLXDC1 may attenuate the progression of colon cancer by direct roles in cancer cells and indirect roles in macrophage polarization, representing a promising therapeutic target for colon cancer patients.
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Biomarcadores de Tumor , Neoplasias del Colon , Macrófagos , Humanos , Neoplasias del Colon/patología , Neoplasias del Colon/metabolismo , Neoplasias del Colon/genética , Biomarcadores de Tumor/metabolismo , Biomarcadores de Tumor/genética , Pronóstico , Macrófagos/metabolismo , Macrófagos/patología , Línea Celular Tumoral , Progresión de la Enfermedad , Receptores de Superficie Celular/metabolismo , Receptores de Superficie Celular/genética , Masculino , Femenino , Proteínas de Neoplasias/metabolismo , Proteínas de Neoplasias/genética , Regulación Neoplásica de la Expresión GénicaRESUMEN
OBJECTIVE: This study investigated the significance of serum hypoxia-inducible factor (HIF)-1α/HIF-2 α and Chitinase 3-Like protein 1 (YKL-40) levels in the assessment of vascular invasion and prognostic outcomes in patients with Follicular Thyroid Cancer (FTC). METHODS: This prospective study comprised 83 patients diagnosed with FTC, who were subsequently categorized into a recurrence group (17 cases) and a non-recurrence group (66 cases). The pathological features of tumor vascular invasion were classified. Serum HIF-1α/HIF-2α and YKL-40 were quantified using a dual antibody sandwich enzyme-linked immunosorbent assay, while serum Thyroglobulin (Tg) levels were measured using an electrochemiluminescence immunoassay method. The Spearman test was employed to assess the correlation between serum factors, and the predictive value of diagnostic factors was determined using receiver operating characteristic curve analysis. A Cox proportional hazards regression model was utilized to analyze independent factors influencing prognosis. RESULTS: Serum HIF-1α, HIF-2α, YKL-40, and Tg were elevated in patients exhibiting higher vascular invasion. A significant positive correlation was observed between Tg and HIF-1α, as well as between HIF-1α and YKL-40. The cut-off values for HIF-1α and YKL-40 in predicting recurrence were 48.25 pg/mL and 60.15 ng/mL, respectively. Patients exceeding these cut-off values experienced a lower recurrence-free survival rate. Furthermore, serum levels surpassing the cut-off value, in conjunction with vascular invasion (v2+), were identified as independent risk factors for recurrence in patients with FTC. CONCLUSION: Serum HIF-1α/HIF-2α and YKL-40 levels correlate with vascular invasion in FTC, and the combination of HIF-1α and YKL-40 predicts recurrence in patients with FTC.
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Adenocarcinoma Folicular , Factores de Transcripción con Motivo Hélice-Asa-Hélice Básico , Biomarcadores de Tumor , Proteína 1 Similar a Quitinasa-3 , Subunidad alfa del Factor 1 Inducible por Hipoxia , Invasividad Neoplásica , Valor Predictivo de las Pruebas , Humanos , Proteína 1 Similar a Quitinasa-3/sangre , Femenino , Masculino , Subunidad alfa del Factor 1 Inducible por Hipoxia/sangre , Persona de Mediana Edad , Pronóstico , Adulto , Adenocarcinoma Folicular/sangre , Adenocarcinoma Folicular/patología , Adenocarcinoma Folicular/mortalidad , Estudios Prospectivos , Factores de Transcripción con Motivo Hélice-Asa-Hélice Básico/sangre , Biomarcadores de Tumor/sangre , Neoplasias de la Tiroides/sangre , Neoplasias de la Tiroides/patología , Neoplasias de la Tiroides/mortalidad , Anciano , Recurrencia Local de Neoplasia/sangre , Recurrencia Local de Neoplasia/patología , Ensayo de Inmunoadsorción Enzimática , Valores de Referencia , Adulto Joven , Estadísticas no Paramétricas , Curva ROCRESUMEN
Information on the potential role of the long non-coding RNA LNC-POTEM-4 in cancer progression is limited. Our preliminary study found that LNC-POTEM-4 was overexpressed in hepatocellular carcinoma (HCC) tissues, which led us to further investigate the biological function and molecular mechanism of LNC-POTEM-4 in HCC development. LNC-POTEM-4 expression in HCC tissues was examined using transcriptome sequencing and quantitative reverse transcription PCR. The relationships between LNC-POTEM-4 and the stage and prognosis of HCC in patient data from the TCGA database were analyzed. The effects of LNC-POTEM-4 on proliferation, invasion/migration, and epithelial-mesenchymal transition marker expression in HCC cells were evaluated in vitro using gain- and loss-of-function assays, while its effects on tumor growth and metastasis were explored through animal experiments. A LNC-POTEM-4/microRNA (miR)-149-5p/Wnt4 regulatory signaling axis was identified using bioinformatics analysis, and dual luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays. Co-transfection of LNC-POTEM-4 and Wnt4 expression plasmids was employed to confirm the new signaling pathway. We found that LNC-POTEM-4 was overexpressed in HCC tissues and was linked to poor staging and prognosis. LNC-POTEM-4 promoted proliferation, invasion, migration, and the epithelial-mesenchymal transition of HCC cells in vitro. Silencing of LNC-POTEM-4 inhibited HCC growth and distant metastasis in vivo. Mechanically, LNC-POTEM-4 was found to function as a competitive endogenous RNA, upregulating Wnt4 by sponging miR-149-5p to promote HCC progression. Wnt4 overexpression may have counteracted the tumor-inhibition effect of LNC-POTEM-4 silencing. In conclusion, LNC-POTEM-4 upregulated Wnt4 to activate the Wnt signaling pathway and stimulate the malignancy tendency of HCC by sponging miR-149-5p, providing a prospective target for the detection and therapy of HCC. However, the effects of LNC-POTEM-4 on the miR-149-5p/Wnt4 signaling axis should be further studied in animal experiments.
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Suppression of roots and/or their symbiotic microorganisms, such as mycorrhizal fungi and rhizobia, is an effective way for alien plants to outcompete native plants. However, little is known about how invasive and native plants interact with the quantity and activity of nutrient-acquisition agents. Here a pot experiment was conducted with monoculture and mixed plantings of an invasive plant, Xanthium strumarium, and a common native legume, Glycine max. We measured traits related to root and nodule quantity and activity and mycorrhizal colonization. Compared to the monoculture, fine root quantity (biomass, surface area) and activity (root nitrogen (N) concentration, acid phosphatase activity) of G. max decreased in mixed plantings; nodule quantity (biomass) decreased by 45%, while nodule activity in N-fixing via rhizobium increased by 106%; mycorrhizal colonization was unaffected. Contribution of N fixation to leaf N content in G. max increased in the mixed plantings, and this increase was attributed to a decrease in the rhizosphere soil N of G. max in the mixed plantings. Increased root quantity and activity, along with a higher mycorrhizal association was observed in X. strumarium in the mixed compared to monoculture. Together, the invasive plant did not directly scavenge N from nodule-fixed N, but rather depleted the rhizosphere soil N of the legume, thereby stimulating the activity of N-fixation and increasing the dependence of the native legume on this N source. The quantity-activity framework holds promise for future studies on how native legumes respond to alien plant invasions.
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Background: The extent of skull base invasion (SBI) in nasopharyngeal carcinoma (NPC) directly impacts tumor staging, treatment strategies, and prognosis assessment for NPC patients, emphasizing the critical need for prompt diagnosis and precise assessment of invasion. Thus, we aimed to integrate the advantages of intravoxel incoherent motion diffusion-weighted imaging (IVIM-DWI) and conventional magnetic resonance imaging (cMRI), and assess their combined diagnostic efficacy versus that of 18F-sodium fluoride (18F-NaF) positron emission tomography/computed tomography (PET/CT) for detecting SBI in NPC patients. Methods: The study prospectively and randomly recruited 62 patients newly diagnosed with NPC by pathological biopsy at the Cancer Center of Affiliated Hospital of Guangdong Medical University from January 2021 to September 2022. All patients underwent baseline cMRI, IVIM-DWI, and PET/CT scans. The IVIM-DWI analysis included 3 primary parameters: true diffusion coefficient (D), pseudodiffusion coefficient (D*), and pseudodiffusion fraction (f). SBI was defined as the involvement of any substructure confirmed by follow-up MRI and clinical symptoms. Inter-observer agreement was evaluated utilizing the intraclass correlation coefficients (ICC) and kappa coefficients. Receiver operating characteristic (ROC) curve was used to evaluate the diagnostic performance of cMRI, IVIM-DWI plus cMRI, and PET/CT. DeLong test was used to compare the areas under the curve (AUC) of the 3 modalities. Results: Excellent inter-observer reliability was observed (range, 0.841-0.946). Among the IVIM-DWI parameters, D* + f demonstrated comparable accuracy to D + D* + f (AUC 0.906 vs. 0.904; sensitivity 88.9% vs. 89.8%; specificity 92.3% vs. 91.0%). IVIM-DWI plus cMRI yielded an overall AUC of 0.947, sensitivity of 92.6%, and specificity of 96.8%, surpassing cMRI alone with an AUC of 0.914 (P=0.025), sensitivity of 91.2%, and specificity of 91.7%, as well as 18F-NaF PET/CT with an AUC of 0.852 (P<0.001), sensitivity of 80.1%, and specificity of 90.4%. In detecting substructures of SBI, IVIM-DWI plus cMRI showed superior performance compared to 18F-NaF PET/CT within the petrous part of the temporal bone (AUC 0.968 vs. 0.871, P=0.011; sensitivity 93.5% vs. 87.1%, specificity 100% vs. 87.1%), pterygopalatine fossa (AUC 0.935 vs. 0.831, P=0.032; sensitivity 93.9% vs. 69.7%, specificity 93.1% vs. 96.6%), and foramen ovale (AUC 0.885 vs. 0.710, P=0.019; sensitivity 76.9% vs. 61.5%, specificity 100% vs. 80.6%). Conclusions: IVIM-DWI plus cMRI can accurately detect SBI and the substructures in NPC, providing a valuable reference for personalized treatment strategies and precise prognosis assessment.
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Background: Breast cancer (BC) is the leading cancer in women globally, with human epidermal growth factor receptor 2 (HER2)-positive subtype accounting for 15-20% of cases and exhibiting aggressive behavior. The standard of care for operable BC has evolved to include neoadjuvant systemic therapy, which can guide treatment decisions and improve outcomes, particularly in HER2+ BC. This study aims to investigate whether axillary ultrasound has a good negative predictive value (NPV) for early HER2 BC patients and to identify clinicopathological factors that can impact the axillary lymph node metastasis. Methods: This retrospective, single-center study evaluated the medical records of 135 patients with HER2+ BC, cT ≤3 cm, and clinically negative axillary lymph nodes from 2018 to 2020. The study aimed to determine the NPV of axillary ultrasound for pathologically negative axillary lymph node status and to identify factors associated with axillary lymph node metastasis. Results: The NPV of axillary ultrasound was 78.5%, increasing to 89.6% and 93.3% when considering 0-1 and 0-2 metastatic lymph nodes, respectively. Lymphovascular invasion (LVI) was significantly associated with axillary lymph node metastasis, with a 2.2-fold increased risk. Conclusions: Axillary ultrasound shows good predictive value for axillary lymph node negativity in HER2+ BC patients with small tumors. However, the presence of LVI increases the risk of metastasis, suggesting a need for neoadjuvant chemotherapy. These findings contribute to personalized treatment strategies for early HER2+ BC, emphasizing the role of axillary ultrasound in clinical decision-making.
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Background: Papillary thyroid carcinoma (PTC) is the most common malignant tumor of the thyroid gland, with lymph node metastasis significantly affecting patient prognosis. In recent years, body mass index (BMI) has garnered widespread attention as a potential factor influencing cancer development. This study aimed to explore the relationship between BMI and lymph node metastasis in patients with PTC, particularly focusing on the risk of metastasis in the lateral and central neck compartments. Methods: This retrospective study comprised 993 patients who underwent surgical treatment and were pathologically confirmed to have PTC. Patient BMI data were collected, and their relationship with lymph node metastasis in the lateral and central neck compartments was analyzed. Logistic regression models were employed to analyze the correlation between BMI and lymph node metastasis. Results: The study found a significant correlation between BMI and the risk of lateral neck lymph node metastasis in patients (P=0.008), along with a corresponding increase in extrathyroidal extension risk (P=0.02). While elevated BMI did not directly increase the risk of central compartment metastasis, a significant increase was observed in the number of central compartment lymph node metastases (P=0.009) and their proportion among the total central compartment lymph nodes (P=0.01) in patients with higher BMI. Additionally, multifocality, age, and gender were identified as risk factors for lateral neck lymph node metastasis, whereas Hashimoto's thyroiditis did not exhibit a similar impact. Conclusions: This study highlights that higher BMI is an important risk factor for lateral neck lymph node metastasis in patients with PTC and may exacerbate the severity of central compartment lymph node metastasis. These findings underscore the importance of considering BMI in the management of thyroid cancer and provide data support for future prevention and intervention strategies.
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Fusobacterium nucleatum is an anaerobic commensal of the oral cavity recently reported to be associated with cancers of the gastrointestinal tract and oral squamous cell carcinoma (OSCC). In this study, we investigate the impact on oral keratinocytes of infection with a genetically diverse set of strains of F. nucleatum subsp. polymorphum recovered from patients with oral dysplasia (n=6). We employed H357 oral keratinocytes derived from a stage 1 OSCC and H376 cells derived from a stage 3 OSCC. Adhesion phenotypes were strain specific, with 3/6 clinical isolates examined exhibiting higher adherence to the stage 3 H376 cell line. Conversely, intracellular invasion was greatest in the H357 cells and was associated with specific transcriptional responses including autophagy and keratinization. Infection of both H357 and H376 cell lines induced transcriptional and cytokine responses linked to cancer cell migration and angiogenesis. F. nucleatum infection induced greater levels of MMP9 secretion in the H376 cell line which was associated with enhanced motility and invasion phenotypes. Additionally, the degree of F. nucleatum induced invasive growth by H376 cells varied between different clinical isolates of F. nucleatum subsp. polymorphum. Blockage of CCL5 signalling using the inhibitor metCCL5 resulted in reduced keratinocyte invasion. F. nucleatum infection also induced expression of the pro-angiogenic chemokine MCP-1 and the angiogenic growth factor VEGF-A resulting in increased capillary-like tube formation in HUVEC cells, most significantly in H376 cells. Treatment of HUVEC cells with resveratrol, a VEGF-A signalling inhibitor, significantly attenuated F. nucleatum induced tube formation. Our data indicate that the outcomes of F. nucleatum-oral cell interactions can vary greatly depending on the bacterial genotype and the malignant phenotype of the host cell.
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Infecciones por Fusobacterium , Fusobacterium nucleatum , Queratinocitos , Neoplasias de la Boca , Humanos , Fusobacterium nucleatum/patogenicidad , Queratinocitos/microbiología , Neoplasias de la Boca/microbiología , Neoplasias de la Boca/patología , Infecciones por Fusobacterium/microbiología , Línea Celular Tumoral , Movimiento Celular , Adhesión Bacteriana , Carcinoma de Células Escamosas/microbiología , Carcinoma de Células Escamosas/patología , Neovascularización Patológica/microbiología , Metaloproteinasa 9 de la Matriz/metabolismo , Metaloproteinasa 9 de la Matriz/genética , Citocinas/metabolismo , Factor A de Crecimiento Endotelial Vascular/metabolismo , Boca/microbiologíaRESUMEN
Background and aim: Accurately predicting microvascular invasion (MVI) before surgery is beneficial for surgical decision-making, and some high-risk hepatocellular carcinoma (HCC) patients may benefit from postoperative adjuvant transarterial chemoembolization (PA-TACE). The purpose of this study was to develop and validate a novel nomogram for predicting MVI and assessing the survival benefits of selectively receiving PA-TACE in HCC patients. Methods: The 1372 HCC patients who underwent hepatectomy at four medical institutions were randomly divided into training and validation datasets according to a 7:3 ratio. We developed and validated a nomogram for predicting MVI using preoperative clinical data and further evaluated the survival benefits of selective PA-TACE in different risk subgroups. Results: The nomogram for predicting MVI integrated alpha-fetoprotein, tumor diameter, tumor number, and tumor margin, with an area under the curve of 0.724, which was greater than that of any single predictive factor. The calibration curve, decision curve, and clinical impact curve demonstrated that the nomogram had strong predictive performance. Risk stratification based on the nomogram revealed that patients in the low-risk group did not achieve better DFS and OS with PA-TACE (all p > 0.05), while patients in the medium-to-high risk groups could benefit from higher DFS (Medium-risk, p = 0.039; High-risk, p = 0.027) and OS (Medium-risk, p = 0.001; High-risk, p = 0.019) with PA-TACE. Conclusions: The nomogram predicting MVI demonstrated strong predictive performance, and its risk stratification aided in identifying different subgroups of HCC patients who may benefit from PA-TACE with improved survival outcomes.
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Plant-associated microbial communities are crucial for plant growth and health. However, assembly mechanisms of microbial communities and microbial interaction patterns remain elusive across vary degrees of pathogen-induced diseases. By using 16S rRNA high-throughput sequencing technology, we investigated the impact of wildfire disease on the microbial composition and interaction network in plant three different compartments. The results showed that pathogen infection significantly affect the phyllosphere and rhizosphere microbial community. We found that the primary sources of microbial communities in healthy and mildly infected plants were from the phyllosphere and hydroponic solution community. Mutual exchanges between phyllosphere and rhizosphere communities were observed, but microbial species migration from the leaf to the root was rarely observed in severely infected plants. Moreover, wildfire disease reduced the diversity and network complexity of plant microbial communities. Interactions among pathogenic bacterial members suggested that Caulobacter and Bosea might be crucial "pathogen antagonists" inhibiting the spread of wildfire disease. Our study provides deep insights into plant pathoecology, which is helpful for the development of novel strategies for phyllosphere disease prediction or prevention.
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Alien plant invasion success can be inhibited by two key biotic factors: native herbivores and plant diversity. However, few studies have experimentally tested whether these factors interact to synergistically resist invasion success, especially factoring in changing global environments (e.g. nutrient enrichment). Here we tested how the synergy between native herbivores and plant diversity affects alien plant invasion success in various nutrient conditions. For this purpose, we exposed alien plant species in pot-mesocosms to different levels of native plant diversity (4 vs. 8 species), native generalist herbivores, and high and low soil nutrient levels. We found that generalist herbivores preferred alien plants to native plants, inhibiting invasion success in a native community. This inhibition was amplified by highly diverse native communities. Further, the amplified effect between herbivory and native plant diversity was independent of nutrient conditions. Our results suggest that a higher diversity of native communities can strengthen the resistance of native generalist herbivores to alien plant invasions by enhancing herbivory tolerance. The synergistic effect remains in force in nutrient-enriched habitats that are always invaded by alien plant species. Our results shed light on the effective control of plant invasions using multi-trophic means, even in the face of future global changes.
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PURPOSE: Abnormal cell death due to superficial trophoblast dysfunction caused by placental hypoxia plays a vital role in the development of preeclampsia (PE). Lactic acid stimulates gene transcription in chromatin through lactate modification of histone lysine. Nevertheless, the content and function of lactate in PE development remains largely unclear. METHODS: The contents of lactic acid and copper in 30 PE and 30 normal placentas were determined by kit colorimetry. Real-time quantitative fluorescent PCR (qRT-PCR) and Western blot were used to detect the expression of SLC31A1 in cells and tissues. Cell proliferation, apoptosis, and invasion were detected by cell counting kit 8 (CCK-8), MTS assay, colony formation assay, and Transwell assay. The transcriptional regulation between Grhl2 and SLC31A was verified by the luciferase reporter gene method and ChIP. The H3K18la modification level was detected by ChIP-PCR. RESULTS: Herein, we detected increased lactic acid levels in the PE placental tissue, which inhibit the proliferation and invasion of trophoblasts. Interestingly, lactic acid increases intracellular copper content by enhancing the expression of SLC31A1, a key protein of copper ion transporters. Lentivirus knockdown of SLC31A1 blocked the lactate-induced proliferation and invasion of trophoblasts by inhibiting cell cuproptosis. Mechanically, we identified that Grhl2 mediated SLC31A1 expression through transcription and participated in SLC31A1-inhibited proliferation, invasion, and cuproptosis of trophoblasts. Furthermore, the high lactate content increased Grhl2 expression by enhancing lactate modification of histone H3K18 in the Grhl2 promoter region. CONCLUSIONS: Blocking the lactate-regulated Grhl2/SLC31A1 axis and trophoblastic cuproptosis may be a potential approach to prevent and treat PE.
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Microbial communities are undergoing unprecedented dispersion and amalgamation across diverse ecosystems, thereby exerting profound and pervasive influences on microbial assemblages and ecosystem dynamics. This review delves into the phenomenon of community coalescence, offering an ecological overview that outlines its four-step process and elucidates the intrinsic interconnections in the context of community assembly. We examine pivotal mechanisms driving community coalescence, with a particular emphasis on elucidating the fates of both source and resident microbial communities and the consequential impacts on the ecosystem. Finally, we proffer recommendations to guide researchers in this rapidly evolving domain, facilitating deeper insights into the ecological ramifications of microbial community coalescence.
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BACKGROUND: Desmoid tumors, also known as aggressive fibromatosis, are rare benign tumors originating from the musculoaponeurotic stroma. While desmoid tumors in the head and neck region are documented, those located in the nasopharynx are exceptionally rare. CASE PRESENTATION: A 26-year-old male presented with a three-year history of left nasal obstruction. A CT scan revealed a mass measuring 5.9 × 4.6 × 3.2 cm occupying the left nasal cavity and nasopharynx, with invasion into the maxillary sinus wall. A biopsy confirmed the presence of a nasopharyngeal desmoid tumor. The patient subsequently underwent endoscopic resection followed by radiotherapy. DISCUSSION: Nasopharyngeal desmoid tumors pose a significant diagnostic challenge due to their rarity. The use of MRI and CT scans is crucial for accurate diagnosis, despite their histologically benign nature. It is important to note that these tumors can mimic malignant lesions, emphasizing the necessity for a thorough and meticulous evaluation during the diagnostic process. CONCLUSION: This case underscores the diagnostic and therapeutic complexities associated with nasopharyngeal desmoid tumors. Increased reporting and documentation of such cases are essential to enhance the understanding and management of this rare condition.
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Uterine cancer is the most common gynecologic malignancy in the United States, with endometrioid endometrial adenocarcinoma (EC) being the most common histologic sub-type. Considering the molecular classifications of EC, efforts have been made to identify additional biomarkers that can assist in diagnosis, prognosis, and individualized therapy. We sought to explore the relationship of Repressor Element 1 (RE1) silencing transcription factor (REST), which downregulates neuronal genes in non-neuronal tissue, along with matrix metalloproteinase-24 (MMP24) and EC. We analyzed the expression of REST and MMP24 in 31 cases of endometrial cancer and 16 controls. We then explored the baseline expression of REST and MMP24 in two EC cell lines (Ishikawa and HEC-1-A) compared to a benign cell line (t-HESC) and subsequently evaluated proliferation, migration, and invasion in the setting of loss of REST gene expression. REST and MMP24 expression were significantly lower in human EC samples compared to control samples. REST was highly expressed in EC cell lines, but decreasing REST gene expression increased proliferation (FC: 1.13X, p < 0.0001), migration (1.72X, p < 0.0001), and invasion (FC: 7.77X, p < 0.05) in Ishikawa cells, which are hallmarks of cancer progression and metastasis. These findings elicit a potential role for REST as a putative tumor suppressor in EC.
Asunto(s)
Movimiento Celular , Proliferación Celular , Neoplasias Endometriales , Regulación Neoplásica de la Expresión Génica , Proteínas Represoras , Humanos , Neoplasias Endometriales/genética , Neoplasias Endometriales/metabolismo , Neoplasias Endometriales/patología , Femenino , Proteínas Represoras/genética , Proteínas Represoras/metabolismo , Línea Celular Tumoral , Proliferación Celular/genética , Movimiento Celular/genética , Persona de Mediana Edad , Genes Supresores de Tumor , Anciano , Biomarcadores de Tumor/genética , Biomarcadores de Tumor/metabolismo , Invasividad NeoplásicaRESUMEN
Placenta accreta spectrum (PAS) disorders are characterized by abnormal trophoblastic invasion into the myometrium, leading to significant maternal health risks. PAS includes placenta accreta (invasion < 50% of the myometrium), increta (invasion > 50%), and percreta (invasion through the entire myometrium). The condition is most associated with previous cesarean deliveries and increases in chance with the number of prior cesarians. The increasing global cesarean rates heighten the importance of early PAS diagnosis and management. This review explores genetic expression and key regulatory processes, such as apoptosis, cell proliferation, invasion, and inflammation, focusing on signaling pathways, genetic expression, biomarkers, and non-coding RNAs involved in trophoblastic invasion. It compiles the recent scientific literature (2014-2024) from the Scopus, PubMed, Google Scholar, and Web of Science databases. Identifying new biomarkers like AFP, sFlt-1, ß-hCG, PlGF, and PAPP-A aids in early detection and management. Understanding genetic expression and non-coding RNAs is crucial for unraveling PAS complexities. In addition, aberrant signaling pathways like Notch, PI3K/Akt, STAT3, and TGF-ß offer potential therapeutic targets to modulate trophoblastic invasion. This review underscores the need for interdisciplinary care, early diagnosis, and ongoing research into PAS biomarkers and molecular mechanisms to improve prognosis and quality of life for affected women.