RESUMO

Anti-double-stranded DNA antibodies (anti-dsDNA) serve as a crucial serological indicator for systemic lupus erythematosus (SLE). Chemiluminescent immunoassay (CIA) is mainly used in clinical diagnosis of SLE, but suffers from low specificity, partially because the use of dsDNA antigens of varied sources in current CIA kits that sometimes led to controversial results. On the basis that anti-dsDNA in healthy individuals tend to selectively bind with dsDNA originating from pathogens, whereas pathogenic anti-dsDNA in SLE patients bind all forms of dsDNA, here we proposed the use of dsDNA fragment derived from human genome as antigen (synthesized via PCR using the human genomic DNA as the template). A magnetic bead-based immunofluorescence assay (IFA) was thus developed for SLE diagnosis, which exhibited improved sensitivity and specificity over CIA using the WHO reference reagent (15/174) as standard. For clinical serum sample analysis (n = 590), IFA exhibited an accuracy of 71.9% that was higher than CIA (65.3%). Crucially, the IFA results exhibited stronger correlations with the activity of SLE, renal involvement, and its prognosis. Besides the improved clinical diagnosis, the proposed IFA also holds great promise in assay standardization due to the high homogeneity of the synthetic dsDNA.

RESUMO

Rice blast is one of the most hazardous diseases affecting rice production. Previously, we discovered that the Atp2 protein of Rhodopseudomonas palustris could significantly inhibit the appressorium formation and pathogenicity of Magnaporthe oryzae. However, the molecular mechanism of this fungus has remained unknown. This study revealed that Atp2 can enter the cell and interact with the ribosomal protein MoRpl12 of M. oryzae, directly affecting the expression of the MoRpl12 protein. Silencing the MoRPL12 gene can affect cell wall integrity, growth, conidiogenesis, and fungal pathogenicity. The quantitative reverse transcription PCR results showed significant changes in the expression of conidiation-related genes in the MoRPL12 gene-silenced mutants or in the Atp2 protein-treated plants. We further found that Atp2 treatment can influence the expression of ribosomal-related genes, such as RPL, in M. oryzae. Our study revealed a novel antifungal mechanism by which the Atp2 protein binds to the ribosomal protein MoRpl12 and inhibits the pathogenicity of rice blast fungus, providing a new potential target for rice blast prevention and control.

RESUMO

AIM: To the determinants and the underlying mechanism of health literacy, social support, and resilience on the health-related quality of life (HRQoL) among older stroke survivors. DESIGN: A cross-sectional design was applied at four comprehensive hospitals in Chongqing via convenience sampling from January 2020 to June 2021. METHODS: Health literacy, social support, and resilience were designed as independent variables, and HRQoL was measured as a dependent variable. Structural equation modelling with the bootstrap method was used to test the hypotheses. RESULTS: The theoretically derived model exhibited a good fit (χ2/df ratio = 2.830, GFI = 0.987, CFI = 0.978, RMSEA = 0.066). Health literacy (ß = 0.12, p < 0.05) and social support (ß = 0.14, p < 0.05) directly affect HRQoL. Resilience (ß = 0.40, p < 0.01) also mediated the relationship between health literacy, social support, and HRQoL. The three variables explaining 29.0% of HRQoL variance. PATIENT OR PUBLIC CONTRIBUTION: There was no direct patient or public involvement in the design, conduct, or reporting of this study. Participants were recruited through convenience sampling from four comprehensive hospitals in Chongqing, and their perspectives or contributions were not explicitly sought. The study focused on examining the determinants and underlying mechanism of health literacy, social support, and resilience on the health-related quality of life among older stroke survivors. Nonetheless, the findings of this research may inform the development of interventions aimed at improving the health-related quality of life in post-stroke older patients.

Assuntos

RESUMO

A thermoresponsive molecularly imprinted hydrogel sensor was constructed for the specific selective recognition of enterovirus 71 (EV71). Due to the introduction of the thermosensitive monomer N-isopropylacrylamide (NIPAM), when the imprinted hydrogel is incubated with the virus at 37℃, the surface specific imprinting cavity will specifically recognize and capture the target virus EV71. When the temperature rises to 45℃, the combined EV71 is rapidly released due to changes in the shape and function of the imprinted sites. The MIP hydrogel-based viral sensor developed recognized, captured, and released the target virus in a non-invasive way. The imprinting factor of the target virus was 5.2, suggesting high selectivity, and the detection limit was 7.1 fM, suggesting high sensitivity. Detection was rapid, as adsorption equilibrium was achieved within 30 min. This method provides a new sustainable avenue for the simple and rapid detection of viruses.

Assuntos

RESUMO

Hydroxyl radical (HO•) and chlorine atom (Cl•) are common reactive species in aqueous environments. However, the intrinsic difference in their reactions with organic compounds has not been revealed. This study compared the reaction mechanisms of HO• and Cl• with 13 aromatic and 11 aliphatic compounds by quantum chemical calculation and laser flash photolysis. Both HO• and Cl• can spontaneously react with aromatic compounds via radical adduct formation (RAF), hydrogen atom transfer (HAT), and single electron transfer (SET) pathways. The SET reactions of Cl• were more thermodynamically favorable than HO•, but contrary results were obtained for HAT reactions. According to the free energy of activation (ΔGaq‡), the dominant oxidation mechanisms of aromatic compounds were RAF and SET by HO• and SET by Cl•. The important role of SET in the HO• reactions with aromatic compounds was further verified by accurately calculating the solvation free energy of HO•/HO- and experimentally tracking the radical cations, which were generally neglected in previous studies. Meanwhile, the ΔGaq‡ value of each reaction pathway of Cl• was lower than that of HO•, resulting in higher rate constants of Cl• with aromatic compounds than HO•. For saturated aliphatic compounds, HAT was found to be the only mechanism accounting for their transformation by HO• and Cl•. This study proposed general rules for the reaction mechanisms of HO• and Cl• and unraveled their differences in the aspects of thermodynamics and kinetics, providing fundamental information for understanding contaminant transformation in processes involving HO• and Cl•.

RESUMO

AIMS: Fibrocartilaginous dysplasia (FCD) is a subvariant of fibrous dysplasia (FD). This study aims to retrospectively elucidate the clinicopathological and separate genetic features of the cartilaginous and fibro-osseous components of FCD. METHODS: In total, 24 patients (14 men and 10 women) with FCD were included in our cohort. The diagnosis was confirmed morphologically and immunohistochemically, and genetic features were determined via Sanger sequencing. RESULTS: Five patients were polyostotic, and 19 were monostotic, predominantly concerning the femur. Radiography revealed a well-demarcated ground glass appearance with ring-like or scattered calcification. Histologically, the lesions were characterised by proliferative fibroblasts, immature woven bone and highly differentiated hyaline cartilage. The fibro-osseous components exhibited positive immunoreaction with SATB2 and a low Ki-67 proliferation index. The fibro-osseous and cartilaginous components shared mutations at codon 201 in exon 8 of the guanine nucleotide-binding protein/a-subunit (GNAS) gene, specifically CGT>CAT (p.R201H) in four patients and the wild-type isocitrate dehydrogenase (IDH)1/IDH2 gene. Telomerase reverse transcriptase (TERT) promoter mutations (C288T and C229G) occurred in both fibro-osseous and cartilaginous components in two patients. CONCLUSIONS: FCD encompasses areas of conventional FD with additional cartilage. Importantly, the presence or absence of mutations in the GNAS gene and/or the TERT promoter is common between the fibro-osseous and cartilaginous components of the disease. These results further confirmed FCD as a variant of FD.

RESUMO

Gynecological cancers are prevalent malignancies among females, and surgical intervention is the primary therapeutic approach offering the possibility of a definitive cure. Recent research has highlighted the susceptibility of gynecological cancer patients to experiencing anxiety symptoms during the perioperative and postoperative phases, with this psychological condition being linked to suboptimal recovery following surgery. Nevertheless, certain interventions have shown promise in mitigating perioperative and postoperative anxiety in gynecological cancer patients. In this study, we conducted a comprehensive review to collect the existing evidence on this subject. Through a systematic search across six common databases, we screened and included 28 pertinent studies. The current review emphasizes the elevated occurrence of perioperative and postoperative anxiety among patients with gynecological cancers (i.e., uterine, cervical, ovarian, endometrial, and vulval cancers). Specific nursing interventions (i.e., crisis intervention nursing, multidisciplinary collaborative continuous nursing, psychological nursing, comprehensive psychological nursing, reminiscence therapy involved care, cognitive behavioral stress management, hospital-family integrated continuation nursing, high-quality nursing care, relaxation-focused nursing program, and relaxation/counseling intervention) and psychotropic medications may serve as dependable approaches to mitigate perioperative and postoperative anxiety. This study represents a novel contribution to the literature by providing a characterization of perioperative and postoperative anxiety in the context of gynecological oncology. The findings underscore the significance of addressing perioperative and postoperative anxiety as a critical clinical concern for individuals with gynecological cancers, emphasizing the need for further research to develop effective interventions.

RESUMO

AIM: To investigate the levels of information literacy, evidence-based nursing competence and innovative behaviour in specialist nurses, determine the impact of information literacy and evidence-based nursing competence on the innovative behaviour of specialist nurses and to analyse the mediating role of evidence-based nursing competence between information literacy and innovative behaviour among specialist nurses. DESIGN: A multicenter cross-sectional design. METHODS: In March 2024, a survey was conducted on 313 specialist nurses in four tertiary Grade A comprehensive hospitals in China. Data collection involved the utilization of general demographic questionnaire, the Information Literacy Questionnaire, the Evidence-Based Nursing Competence Scale and the Nurse Innovation Behaviour Scale. The data were analysed using IBM SPSS26 and Amos28 software. RESULTS: Specialist nurses scored above average in information literacy, evidence-based nursing competence and innovative behaviour. Information literacy significantly positively correlated with innovative behaviour. Evidence-based nursing competence also positively affected innovative behaviour and partially mediated the relationship between information literacy and innovative behaviour. CONCLUSION: This research indicated that specialist nurses exhibited above-average levels of evidence-based nursing competence, information literacy and innovative behaviour. Both information literacy and evidence-based nursing competence positively impacted innovative behaviour, with evidence-based nursing competence playing a significant mediating role between information literacy and innovative behaviour. IMPACT: The findings suggest that nursing managers should focus on enhancing information literacy and evidence-based nursing competence in specialist nurses. Improving these abilities will support the implementation of innovative practices and advance the nursing field. REPORTING METHOD: The research findings were presented in strict accordance with the STROBE statement. PATIENT OR PUBLIC CONTRIBUTION: Not applicable. CONTRIBUTE TO THE WIDER GLOBAL CLINICAL COMMUNITY: It provides reference guidance and theoretical basis for global nursing managers to formulate targeted interventions, so as to effectively enhance the innovative behaviour of specialist nurses.

RESUMO

Background: Several transcription factors and co-factors are encoded by the RFX (Regulatory Factor X) family (RFX1-8) and associated genes (RFXAP and RFXANK). Increasing evidence suggests that the RFX family and associated genes are involved in the development and progression of cancer. However, no prior research has focused on a multi-omic analysis of these genes to evaluate their role in tumor progression. Methods: Using combined TCGA and GTEx pan-cancer data, we investigated the expression patterns and survival profiles of these ten genes. We then focused on RFX8 to analyze its clinicopathological and therapeutic features. Finally, we conducted experimental validation of RFX8 function in acute myeloid leukemia (AML). Results: RFX5 and RFXANK showed higher expression levels, while RFX6 showed lower expression levels in most types of cancer, with RFX8 being the most upregulated in LAML. RFX2 and RFXAP demonstrated prognostic significance in eight types of cancer, and RFX8 showed significance in six types of cancer. The expression of these ten genes exhibited specific characteristics in immune subtypes, tumor microenvironment, and stemness. The expression of RFX8 was correlated with various tumor stages, microsatellite instability (MSI), tumor mutation burden (TMB), immune cell infiltration, and immune-checkpoint expression. Additionally, RFX8 was found to regulate tumorigenesis and sensitivity to chelerythrine in AML. Conclusions: Our work delineated the landscape of the RFX family and associated genes in the pan-cancer context and the specific role of RFX8 in AML. These findings might offer cues for further investigations of these genes in cancer biology.

RESUMO

To investigate the biomechanical mechanisms underlying the pathogenesis and explore the effects of kinesiology taping (KT) on neuromuscular control in HV patients. The study population consisted of 16 young controls (YC group) and 15 patients with hallux valgus (HV group). All subjects underwent a natural velocity gait assessment. Additionally, 11 patients from the HV group received KT intervention over a period of one month, consisting of 15 sessions administered every other day. After the one-month intervention, these patients underwent a gait assessment and were included in the HV-KT group. The electromyography (EMG) and joint motion were evaluated using non-negative matrix factorization (NNMF) to compare the difference in muscle and kinematic synergy among the three groups. The center of plantar pressure (COP) and ground reaction force (GRF) were measured by the force platform. The number of synergies did not differ within the three groups, but the structure of muscle synergies and kinematic synergies differed in the HV group. The KT intervention (HV-KT group) altered the structure of synergies. The correlation between kinematic synergies and muscular synergies was lower in the HV group than in the YC group, whereas the correlation between the two increased after the KT intervention in the HV group. During gait, the HV group tended to activate more muscles around foot joints to maintain body stability. The visual analogue scale (VAS) scores, hallux valgus angle (HVA), and COP were significantly decreased after the intervention ( [Formula: see text]). HV patients exhibited altered kinematic and muscular synergies structures as well as muscle activation. Also, it weakened the balance and athletic ability of HV patients. KT intervention improved neuromuscular control to provide a better gait performance.

Assuntos

RESUMO

The UV/monochloramine (UV/NH2Cl) process, while efficiently eliminating micropollutants, produces toxic byproducts. This study utilized Fourier transform ion cyclotron resonance mass spectrometry (FT-ICR MS) to investigate molecular-level changes in natural organic matter (NOM) and to disclose formation pathways of nitro(so) and chloro byproducts in the UV/NH2Cl process. The UV/NH2Cl process significantly increased the saturation and oxidation levels and altered the elemental composition of NOM. Using 15N labeling and a screening workflow, nitro(so) byproducts with nitrogen originating from inorganic sources (i.e., reactive nitrogen species (RNS) and/or NH2Cl) were found to exhibit total intensities comparable to those from NOM. RNS, rather than NH2Cl, played a significant role in incorporating nitrogen into NOM. Through linkage analysis, nitro(so) addition emerged as an important reaction type among the 25 reaction types applied. By using phenol as a representative model compound, the nitro byproducts were confirmed to be mainly generated through the oxidation of nitroso byproducts instead of nitration. Machine learning and SHAP analysis further identified the major molecular indices distinguishing nitro(so) and chloro precursors from non-precursors. This study enhances our fundamental understanding of the mechanisms driving the generation of nitro(so) and chloro byproducts from their precursors in complex NOM during the UV/NH2Cl process.

Assuntos

RESUMO

Brain injury after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) is the leading cause of neurological dysfunction and death. This study aimed to explore the mechanism of histone deacetylase 6 (HDAC6) in neurofunctional recovery following CA/CPR in rats. A rat model was established by CA/CPR treatment. Adenovirus-packaged sh-HDAC6 was injected into the tail vein. To evaluate the neurofunction of rats, survival time, neurofunctional scores, serum NSE/S100B, and brain water content were measured and Morris water maze test was performed. HDAC6, microRNA (miR)-138-5p, Nod-like receptor protein 3 (NLRP3), and pyroptotic factor levels were determined by real-time quantitative polymerase chain reaction or Western blot assay. HDAC6 and H3K9ac enrichment on miR-138-5p promoter were examined by chromatin immunoprecipitation. miR-138-5p-NLRP3 binding was analyzed by dual-luciferase reporter assay. NLRP3 inflammasome was activated with nigericin sodium salt. After CPR treatment, HDAC6 was highly expressed, while miR-138-5p was downregulated. HDAC6 downregulation improved neurofunction and reduced pyroptosis. HDAC6 enrichment on the miR-138-5p promoter deacetylated H3K9ac, inhibiting miR-138-5p, and promoting NLRP3-mediated pyroptosis. Downregulating miR-138-5p partially reversed the protective effect of HDAC6 inhibition after CPR. In Conclusion, HDAC6 enrichment on miR-138-5p promoter deacetylated H3K9ac, inhibiting miR-138-5p expression and promoting NLRP3-mediated pyroptosis, worsening neurological dysfunction in rats after CPR.

Assuntos

RESUMO

Hyperproliferative  diseases are the first step for tumor formation; thymidine kinase 1 (TK1) mRNA is closely related to cell proliferation. Therefore, the risk of malignant proliferation can be identified by sensitively detecting the variance in TK1 mRNA concentration, which can be used for tumor auxiliary diagnosis and monitoring tumor treatment. Owing to the low abundance and instability of TK1 mRNA in real samples, the development of a sensitive and fast mRNA detection method is necessary. A DNA nanosensor that can be used for detecting TK1 mRNA based on bipedal 3D DNA walker-driven proximal catalytic hairpin assembly (P-CHA) was developed. P-CHA hairpins were hybridized to a linker DNA strand coupled with magnetic nanoparticles to increase their local concentrations. The bipedal DNA walking on the surface of NPs accelerates reaction kinetics using the proximity effect. Taking advantage of the signal amplification of P-CHA as well as the rapid reaction rate of the DNA walker in 80 min, the proposed sensor detects TK1 mRNA with a low detection limit of 14 pM and may then be applied to clinical diagnosis.

Assuntos

RESUMO

Glycoproteins are difficult to be detected by imprinting strategy due to their low natural abundance, high flexible conformation and large size. Herein, a high-density boric acid modified metal-organic framework (MOF) surface molecularly imprinted polymer (SMIP) resonant light scattering sensor was constructed for the high-sensitivity detection of target glycoproteins. A MOF with large specific surface area was selected as the substrate material to support the boric acid group with high loading density (4.66 %). The introduction of the boric acid group in the SMIP provided a high-affinity binding site for the recognition and binding of glycoproteins. Shallow surface cavities with rapid mass transfer (equilibrium time 20 min) were thus formed by surface imprinting. Furthermore, high sensitivity (limit of detection 15 pM) was achieved at physiological pH (7.4), which was conducive to the detection of glycoproteins with low natural abundance in complex biological samples and maintaining physiological activity.

Assuntos

RESUMO

Although molecular imprinting technology has been widely used in the construction of virus sensors, it is still a great challenge to identify subtypes viruses specifically because of their high similarity in morphology, size and structure. Here, a monoclonal molecular imprinted polymers (MIPs) sensor for recognition of H5N1 is constructed to permit the accurate distinguishing of H5N1 from other influenza A virus (IAV) subtypes. Firstly, H5N1 are immobilized on magnetic microspheres to produce H5N1-MagNPs, then the high affinity nanogel H5N1-MIPs is prepared by solid phase imprinting technique. When H5N1-MIPs is combined with MagNP-H5N1, different concentrations of H5N1 are added for competitive substitution. The quantitative detection of H5N1 is realized by the change of fluorescence intensity of supernatant. As expected, the constructed sensor shows satisfactory selectivity, and can identify the target virus from highly similar IAV subtypes, such as H1N1, H7N9 and H9N2. The sensor was highly sensitive, with a detection limit of 0.58 fM, and a selectivity factor that is comparable to that of other small MIPs sensors is achieved. In addition, the proposed sensor is cheap, with a cost of only RMB 0.08 yuan. The proposed monoclonal sensor provides a new method for the specific recognition of designated virus subtype, which is expected to be used for large-scale screening and accurate treatment of infected people.

Assuntos

RESUMO

Nutrient sensing and adaptation in the placenta are essential for pregnancy viability and proper fetal growth. Our recent study demonstrated that the placenta adapts to nutrient insufficiency through mechanistic target of rapamycin (mTOR) inhibition-mediated trophoblast differentiation toward syncytiotrophoblasts (STBs), a highly specialized multinucleated trophoblast subtype mediating extensive maternal-fetal interactions. However, the underlying mechanism remains elusive. Here, we unravel the indispensable role of the mTORC1 downstream transcriptional factor TFEB in STB formation both in vitro and in vivo. TFEB deficiency significantly impaired STB differentiation in human trophoblasts and placenta organoids. Consistently, systemic or trophoblast-specific deletion of Tfeb compromised STB formation and placental vascular construction, leading to severe embryonic lethality. Mechanistically, TFEB conferred direct transcriptional activation of the fusogen ERVFRD-1 in human trophoblasts and thereby promoted STB formation, independent of its canonical function as a master regulator of the autophagy-lysosomal pathway. Moreover, we demonstrated that TFEB directed the trophoblast syncytialization response driven by mTOR complex 1 (mTORC1) signaling. TFEB expression positively correlated with the reinforced trophoblast syncytialization in human fetal growth-restricted placentas exhibiting suppressed mTORC1 activity. Our findings substantiate that the TFEB-fusogen axis ensures proper STB formation during placenta development and under nutrient stress, shedding light on TFEB as a mechanistic link between nutrient-sensing machinery and trophoblast differentiation.

Assuntos

RESUMO

OBJECTIVES: To explore the impact of hallux valgus (HV) on lower limb neuromuscular control strategies during the sit-to-stand (STS) movement, and to evaluate the effects of Kinesio taping (KT) intervention on these control strategies in HV patients. METHODS: We included 14 young healthy controls (HY), 13 patients in the HV group (HV), and 11 patients in the HV group (HVI) who underwent a Kinesio taping (KT) intervention during sit-to-stand (STS) motions. We extracted muscle and kinematic synergies from EMG and motion capture data using non-negative matrix factorization (NNMF). In addition, we calculated the center of pressure (COP) and ground reaction forces (GRF) to assess balance performance. RESULTS: There were no significant differences in the numbers of muscle and kinematic synergies between groups. In the HV group, knee flexors and ankle plantar flexors were abnormally activated, and muscle synergy D was differentiated. Muscle synergy D was not differentiated in the HVI group. CONCLUSION: Abnormal activation of knee flexors and plantar flexors led to the differentiation of module D in HV patients, which can be used as an indicator of the progress of HV rehabilitation. KT intervention improved motor control mechanisms in HV patients.

Assuntos

RESUMO

Sesquiterpene dimers are mainly found in the Asteraceae family. However, conflicting reports on the structures of these compounds can be found in the literature. Herein, we describe ten sesquiterpene dimers isolated from the flowers of Inula japonica, including configurational revisions of japonicone H (1-1), japonicone D (2-1), inulanolide A (4-1), japonicone X (5-1), and inulanolide F (5-2) to compounds 1, 2, 4, and 5, respectively. Five new related metabolites (3 and 6-9) are also described. Application of GIAO NMR/DP4+ analyses and ECD/OR calculations enabled us to revise the absolute configurations of an additional 13 sesquiterpene dimers isolated from plants of the genus Inula. Compounds 1, 2, 4, and 6 exhibited inhibition of nitric oxide production in lipopolysaccharide activated RAW264.7 macrophages with IC50 values of 4.07-10.00 µM.

Assuntos

RESUMO

Although tyrosine kinase inhibitor (TKI) therapy has markedly improved the survival of people with chronic-phase chronic myeloid leukemia (CML), 20-30% of people still experienced therapy failure. Data from 1,955 consecutive subjects with chronic-phase CML diagnosed by the European LeukemiaNet (ELN) recommendations from 1 center receiving initial TKI imatinib or a second-generation (2G-) TKI therapy were interrogated to develop a clinical prediction model for TKI therapy failure. This model was subsequently validated in 3,454 subjects from 76 other centers. Using the predictive clinical co-variates associated with TKI therapy failure, we developed a model that stratified subjects into low-, intermediate- and high-risk subgroups with significantly different cumulative incidences of therapy failure (p < 0.001). There was good discrimination and calibration in the external validation dataset, and the performance was consistent with that of the training dataset. Our model had the better prediction discrimination than the Sokal and ELTS scores did, with the greater time-dependent area under the receiver-operator characteristic curve (AUROC) values and a better ability to re-defined the risk of therapy failure. Our model could help physicians estimate the likelihood of initial imatinib or 2G-TKI therapy failure in people with chronic-phase CML.

RESUMO

The blast crisis (BC) of chronic myeloid leukemia (CML) has poor efficacy against existing treatments and extremely short survival. However, the molecular mechanism of CML-chronic phase (CP) transformation to CML-BC is not yet fully understood. Here, we show that Lin28B, an RNA-binding protein, acted as an activator enhancing the transformation to CML-BC by mediating excessive cell proliferation. The level of Lin28B expression was apparently elevated in patients with CML-BC compared with newly diagnosed patients with CML-CP. The overexpression of Lin28B promoted the proliferation of leukemia cells. Mechanistically, we identified Lin28B as a DNA-binding protein by binding to the promoter region of miR-181d and upregulating its expression, which inhibited the expression of programmed cell death 4 (PDCD4) by binding to the PDCD4 3'UTR region, thereby enhancing the proliferation of CML cells. Overall, the "Lin28B-miR-181d-PDCD4" regulatory axis promoted CML blast crisis. Implications: Our findings highlight the oncogenic role of Lin28B in CML blast crisis, acting as a DNA-binding protein that transcriptionally upregulates miR-181d expression.

Assuntos