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Objective: To investigate the clinicopathological features, and differential diagnosis of verrucous hemangioma (VH). Methods: Twenty-eight VH cases diagnosed from 2005 to 2020 in Henan Provincial People's Hospital, Zhengzhou, China were analyzed retrospectively. Immunohistochemical studies were used to detect diagnostic markers. The mutation status of PIK3CA (exons 9 and 20) was detected using fluorescence PCR. Results: There were 13 males and 15 females in 28 cases, with the male to female ratio of 1.0∶1.2. There were 25 patients under the age of 18 years. The age range was from 10 months to 56 years (mean, 9.7 years; median, 4.5 years). There were 17 cases occurred in the lower extremities, 7 in the upper extremities and 4 in the trunk. All 28 cases were irregular red patches on the skin, which grew slowly. Some of them were thickened with uneven surface, which was light pink or red-white. Skin lesions of the 7 cases ranged from dark red and reddish brown, with a rough and hard surface. Satellite foci were present. Microscopically, 28 cases had a wide range of pathological features. Dilated, malformed vessels were observed from dermal papilla to deep soft tissue. Among them, the dermal papillary layer was mainly composed of many proliferating and expanding thin-walled capillaries and cavernous blood vessels. Thin-walled small vessels were found in the dermal reticular layer and subcutaneous fascia layer, with no obvious endothelial cell proliferation, occasional papillary hyperplasia, and lobular distribution of the malformed vessels in the fascia layer mixed with the fibroadipose tissue. There was epidermal papillary hyperplasia with hyperkeratosis and parakeratosis, lengthening and mutual fusion of epithelial horns. Immunohistochemistry showed that CD31, CD34, ERG and WT-1 were diffusely and strongly positive. The expression of GLUT-1 was present in superficial dermal vascular endothelial cells, but undetectable in the deep layer. The PIK3CA tests of 13 cases showed that no somatic mutations were found in exons 9 and 20. Twenty-five patients were followed up for 5 months to 10 years. Seven patients underwent multiple surgical resections and plastic surgeries due to the large size, and 8 patients had recurrence. Conclusions: VH is a rare congenital vascular malformation and more commonly occurs in infants and children. It tends to appear in limbs, especially lower limbs and distal limbs. Its morphology and immunophenotype are characteristic and should be distinguished from other vascular malformations and the resolution phase of infant hemangiomas. In about one third of the cases, postoperative recurrence may occur and long-term follow-up is often required.

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Objective: To explore the potential mechanism of sorafenib resistance associated long non-coding RNA (lncRNA-SRLR) promoted invasion and metastasis in U2OS osteosarcoma cells. Methods: We transfected U2OS cells with negative control lentivirus (LV-NC) or lncRNA-SRLR overexpressed lentivirus (LV-over/SRLR) particles. LV-NC and LV-over/SRLR stable transfected cells (U20S/NC and U20S/SRLR) were selected by primary cell culture medium containing puromycin. The mRNA expressions of lncRNA-SRLR and procollagen-lysine, procollagen-lysine 2-oxoglutarate 5-dioxygenase 2 (PLOD2) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The effect of lncRNA-SRLR on the invasion of U2OS cells were determined by wound-healing assay and Transwell migration assay. The effect of SRLR on the interleukin-6 (IL-6) secretion of U2OS cells was evaluated by enzyme-linked immunosorbent assay (ELISA) analysis. The subcellular distribution of SRLR in U2OS cells was detected by fluorescence in situ hybridization (FISH) analysis.The expression of PLOD2 in cells was detected by immunofluorescence (IF). The expressions of PLOD2 and focal adhesion kinase (FAK)/signal transducer and activator of transcription 3 (STAT3) signal pathway related proteins in U2OS/NC and U2OS/SRLR cells were detected by western blotting. Results: qRT-PCR assay showed that mRNA expressions of lncRNA-SRLR and PLOD2 in U2OS/SRLR cells were (3 964.97±0.05) and (2.77±0.11), respectively, significantly higher than those in U2OS/NC cells (P<0.001 or P<0.01). The results of wound-healing and Transwell migration assay showed that over-expression of SRLR markedly promoted the invasion ability of U2OS cells (P<0.05). The result of ELISA analysis showed that the IL-6 secretions in U2OS/NC or U2OS/SRLR cells were (125.38±11.22) pg/ml or (119.97±13.43) pg/ml, without statistical significance (P>0.05). The subcellular distribution assay revealed that lncRNA-SRLR is predominately located in the nucleus. The result of IF showed that compared with U2OS/NC cells, the expression of PLOD2 was up-regulated in U2OS/SRLR cells. The result of western blotting showed that over-expression of SRLR significantly increased the expression levels of PLOD2, phosphorylation (p)-FAK and p-STAT3 in U2OS cells (P<0.01). Conclusion: lncRNA-SRLR promotes invasion and metastasis of osteosarcoma by activating PLOD2-FAK/STAT3 signal axis.

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OBJECTIVE: Renal cell carcinoma (RCC) is the most common kidney malignancy that frequently leads to metastasis. Increasing evidence has shown that long non-coding RNAs (lncRNAs) play crucial roles affecting the progression of RCC. The role of lncRNA DUXAP10 in the evolution of RCC has not been defined yet. This project was designed to clarify the effects of DUXAP10 on the proliferation and tumorigenesis of RCC. PATIENTS AND METHODS: We examined the expression of DUXAP10 in the Cancer Genome Atlas (TCGA) and ONCOMINE oncology databases. Then, we performed quantitative reverse-transcription polymerase chain reaction (qRT-PCR) to evaluate DUXAP10 expression in human RCC tissues and cell lines. The correlation between the expression of DUXAP10 and clinical characteristics of RCC patients was analyzed by univariate and Kaplan-Meier analyses. To unveil the biological function of DUXAP10 in cell cycle progression, cell growth, and invasion of RCC, we conducted knockdown experiments in vitro. qRT- PCR and western blotting assays were performed to further investigate the function of DUXAP10 in cancer biology. RESULTS: The data from TCGA showed that the expression of DUXAP10 was upregulated in tissues of RCC compared with normal tissues. Moreover, ONCOMINE database analysis indicated that high DUXAP10 levels were correlated with high clinical stages, inferior TNM classification, and poor overall survival. Furthermore, the results indicated that knockdown of DUXAP10 remarkably inhibited the RCC cell growth, mobility, and invasion, in association with the upregulation of E-cadherin and downregulation of cyclin D, cyclin E, CDK4, N-cadherin, and vimentin. CONCLUSIONS: Our findings highlight the oncogenic role of DUXAP10 in RCC and that DUXAP10 may serve as a novel predictive biomarker and therapeutic target for RCC.

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Objective: Although stage of disease is one of the main factors affecting the prognosis of gastric cancer, the prognosis of gastric cancer patients with different biological behaviors is also different, indicating that the biological behavior of gastric cancer is also of great significance. This study explores the clinicopathological characteristics of gastric cancer patients with different biological behaviors in the same TMN stage, and analyzes its impact on the prognosis, so as to provide reasonable and reliable evidences for surgical treatment. Methods: A retrospective cohort study was carried out. Clinicopathological data of patients with advanced gastric cancer undergoing radical surgery at Department of Gastrointestinal Surgery, the First Affiliated Hospital of China Medical University from January 1980 to December 2012 were collected. Case inclusion criteria: (1) advanced gastric cancer confirmed by postoperative pathology; (2) R0 resections; (3) complete follow-up data. Exclusion criteria: (1) history of previous gastric surgery, preoperative adjuvant therapy, and imaging evidence of distant metastasis before surgery; (2) age of patients <18 or > 90 years; (3) lack of clinical, pathological, or follow-up data. Cumulative survival was analyzed and plotted by the Kaplan-Meier method. Log-rank test was used for univariate analysis and Cox proportional hazard regression was used for multivariate analysis. Difference of prognosis was compared among different biological behaviors at the same TNM stage. Results: A total of 2522 patients were enrolled, including 246 cases in stage IB (T2N0M0), 422 cases in stage IIA, 474 cases in stage IIB, 681 cases in stage IIIA, 441 cases in stage IIIB, and 256 cases in stage IIIC. Their 5-year survival rates were 79.9%, 68.5%, 56.1%, 39.5%, 22.5%, and 8.1%, respectively, and the difference was statistically significant (P<0.001). Univariate and multivariate analysis showed that for patients with stage IB gastric cancer, the macroscopic type as infiltration (HR=1.806, 95% CI:1.174-2.780, P=0.007), tissue growth mode as diffusion (HR=1.370, 95% CI:1.007-1.864, P=0.045), and positive lymphovascular cancer embolus (HR=2.073, 95% CI: 1.333-3.224, P=0.001) were independent risk factors of prognosis; for patients with stage IIA gastric cancer, the macroscopic type as infiltration (HR=1.376, 95% CI: 1.008-1.878, P=0.044), tissue growth mode as diffusion (HR=1.263, 95% CI: 1.061-1.505, P=0.009), positive lymphovascular cancer embolus (HR=2.296, 95% CI:1.753-3.008, P<0.001) were independent risk factors of prognosis; for patients with stage IIB gastric cancer, macroscopic type as infiltration (HR=1.445, 95% CI: 1.056-1.976, P=0.021), positive lymphovascular cancer embolus (HR=1.528, 95% CI: 1.194-1.955, P=0.001) were independent risk factors of prognosis; for patients with stage IIIA gastric cancer, macroscopic type as infiltration (HR=1.395, 95% CI: 1.095-1.777, P=0.007), positive lymphovascular cancer embolus (HR=1.583, 95% CI: 1.315-1.905, P<0.001) and serosal type (tendon type+colorful diffusion type) (HR=1.188, 95% CI: 1.102-1.282, P<0.001) were independent risk factors of prognosis; for patients with stage IIIB gastric cancer, macroscopic type as infiltration (HR=1.485, 95% CI: 1.063-2.076, P=0.021), positive lymphovascular cancer embolus (HR=1.315, 95% CI: 1.060-1.631, P=0.013), and serosal type (tendon type+colorful diffusion type) (HR=1.146, 95% CI: 1.052-1.248, P=0.002) were independent risk factors of prognosis; for patients with stage IIIC gastric cancer, macroscopic type as infiltration (HR=2.986, 95% CI: 1.293-6.898, P=0.010) and serosal type (tendon type+colorful diffusion type) (HR=1.135, 95% CI: 1.003-1.283, P=0.045) were independent risk factors of prognosis. Conclusion: Under the same TNM stage, different biological behaviors have very different prognosis, which indicates that the biological behavior of gastric cancer is equally as important as TNM staging for the prognosis of patients and the guidance of individualized treatment.

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Objective: To investigate the effects of osimertinib on proliferation, migration and invasion of procollagen-lysine 2-oxoglutarate 5-dioxygenase 2 (PLOD2) overexpressing HCC827 cells and explore the potential mechanism of PLOD2 induced osimertinib resistance. Methods: We transfected HCC827 cells with LV-vector and LV-over/PLOD2. The expression of PLOD2 was detected by quantitative real time polymerase chain reaction (qRT-PCR) and western blotting. The effects of osimertinib on the proliferation of HCC827-vector and HCC827-PLOD2 cells were evaluated by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H tetrazolium bromide (MTT) assay. The effects of osimertinib on the migration and invasion of HCC827-vector and HCC827-PLOD2 cells were determined by Transwell assays. The expressions of E-cadherin and vimentin in cells were detected by immunofluorescence (IF). The expressions of epithelial-mesenchymal transition (EMT), FAK-PI3K/AKT and MAPK signal pathway related proteins were detected by western blotting. Results: The MTT assay showed that HCC827-PLOD2 cells were hyposensitive to osimertinib. The 50% inhibitory concentration (IC(50)) and resistance index of osimertinib for HCC827-PLOD2 cells was over 1 000 nmol/L and over 100, respectively. The result of wound healing assay showed that the migration distance of HCC827-PLOD2 was about (2.13±0.21) fold changes as that of HCC827-vector cells. The result of Transwell assay showed that the numbers of HCC827-PLOD2 passing through the matrix membrane were (212.78±10.43), significantly higher than (101.32±12.52) of HCC827-vector cells (P<0.01). The result of IF showed that compared with HCC827-vector cells, the expression of E-cadherin was down-regulated while vimentin was up-regulated in HCC827-PLOD2 cells. Osimertinb downregulated E-cadherin and upregulated vimentin expression in HCC827-vector cells but had limited effect in HCC827-PLOD2 cells. The result of western blotting showed that PLOD2 significantly increased vimentin expression level while decreased E-cadherin expression level. Osimertinib inhibited the expression of p-EGFR, but did not affect the expressions of PLOD2, p-FAK, p-AKT, p-ERK, vimentin and E-cadherin in HCC827-PLOD2 cells. Conclusion: PLOD2 confers resistance to osimertinib in HCC827 cells by regulating EMT, FAK-PI3K/AKT and MAPK signal pathways.

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Comprehensive treatment of gastric cancer is mainly based on the pathological staging. The T stage mainly depends on the accurate determination of the depth of the tumor invasion. The accurate T stage should be standardized pathological examination and continuous sectioning. N stage may be influenced by the number of lymph node examined. Insufficient lymph node examined may lead to stage migration. Therefore, standardizing lymph node dissection and lymph node harvest after surgery is important. M stage is mainly to improve the detection rate of peritoneal lavage cytology (CY), identify high risk factors for peritoneal metastasis, and optimize the prediction of peritoneal metastasis molecular markers, as a complementary methods of clinical examination. Currently, the quality of standardized pathological diagnosis of gastric cancer in China still needs to be improved. This article mainly elucidates the related studies and clinical experience of our center on how to do better in the optimization of gastric cancer TNM staging and pathological quality control.

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Objective: To investigate the clinical and pathologic features, diagnosis and differential diagnosis of hypertrophic port-wine stain (PWS). Methods: Cases of hypertrophic PWS, collected from Henan Provincial People's Hospital between 2012 and 2018, were retrospectively analyzed for their clinical and pathologic features, immunophenotype and histochemical data, and the relevant literature was reviewed. Results: Twenty-four cases of PWS were included in this cohort, located in the head and neck region (20 cases), limbs (2 cases), and trunk (2 cases). The clinical presentations were mainly red or purple-red plaques or slow growing, painless nodules, or thickened and raised above the skin surface. Microscopically, deformed blood vessels showed honeycomb-like, plexiform or cluster-like growth pattern, and diffusely involved the dermis, skin appendages, subcutaneous fat tissue, and deep skeletal muscles; The vascular lumen of the deformed vessels was dilated (≥100 µm in diameter), and in 18 cases the lumen was greater than 400 µm. The superficial dermis mainly contained few deformed capillaries. The deep wall showed thickening of blood vessel wall and fibrous tissue hyperplasia. Elastic fiber and Masson staining indicated abnormal venous vessel, which in some cases contained small amount of abnormal arterioid vessel,without vascular endothelial cell proliferation in all cases. In 24 cases, 19 cases had epidermal atrophy, 6 with vascular chronic inflammation or epidermal ulcer, 4 with capillary hemangioma, 4 with sebaceous gland hyperplasia, 2 with epidermal papillary hyperplasia and 2 with vascular keratomas. Conclusions: PWS is a common congenital capillary malformation. The number of histologically deformed capillaries is reduced and they usually locate in the superficial part. The deep vascular wall is increased with thick venous malformation, diffusely involving the dermis and deep skeletal muscle. Furthermore, PWS needs to be differentiated from infantile hemangioma, cavernous hemangioma and vascular keratomas.

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OBJECTIVE: The aim of this study was to explore the expression of long non-coding RNA (lncRNA) FAM83H-AS1 and its clinical significance in ovarian cancer (OC). PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine the expression level of lncRNA FAM83H-AS1 in 100 pairs of OC tissues and para-cancerous specimens. Meanwhile, the relationship between lncRNA FAM83H-AS1 expression and clinical features of OC patients was analyzed. According to the mean expression level of lncRNA FAM83H-AS1 (3.693), OC patients were divided into two groups, including the high-expression group (n=48) and low-expression group (n=52). After that, the association between lncRNA FAM83H-AS1 expression and clinicopathological features of OC patients was analyzed. Moreover, the correlation between the expression level of lncRNA FAM83H-AS1 and the survival time of patients was estimated using the Kaplan-Meier method. After OVCAR-3 cells were transfected with Si-FAM83H-AS1 or si-NC, the expression of FAM83H-AS1 in OVCAR-3 cells was detected by qRT-PCR. RESULTS: First, qRT-PCR was used to detect the expression of lncRNA FAM83H-AS1 in OC tissues and cell lines. The results showed that lncRNA FAM83H-AS1 was significantly up-regulated in both OC tissues and OC cells when compared with normal controls. Meanwhile, lncRNA FAM83H-AS1 expression was correlated with tumor pathological grade, FIGO stage and distant metastasis of OC patients. Survival analysis was performed by the Kaplan-Meier method. The results indicated that the overall survival time of patients with higher lncRNA FAM83H-AS1 expression was markedly shorter than those with lower lncRNA FAM83H-AS1 expression. In addition, down-regulation of lncRNA FAM83H-AS1 by si-FAM83H-AS1 transfection could remarkably inhibit proliferation and invasion of OC cells in vitro. CONCLUSIONS: LncRNA FAM83H-AS1 was a novel factor involved in OC progression. Our findings suggested that FAM83H-AS1 could serve as a potential biomarker and therapeutic target for OC.

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OBJECTIVE: Long non-coding RNA DUXAP10 plays a significant role in the tumorigenesis and development of human cancer. The present study was performed to investigate the role of DUXAP10 in biological functions and underlying molecular mechanisms of prostate cancer cells. MATERIALS AND METHODS: First, the quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to detect the expression of DUXAP10 in human prostate cancer cell lines 22RV1, PC3, and DU145. Subsequently, small interfering RNAs (siRNAs) targeting at DUXAP10 mRNA were used to downregulate DUXAP10 expression. Then, the biological functions of DUXAP10 in prostate cancer cells, proliferation, migration, and apoptosis were studied by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony-formation assay, cell cycle analysis, transwell migration assay, wound healing assay, and cell apoptosis assay, respectively. Finally, qRT-PCR analysis and Western blot assay were used to investigate the molecular mechanisms of DUXAP10 underlying the progression of prostate cancer. RESULTS: Results showed that the expression of DUXAP10 was higher in PC3 and DU145 cell lines than that in the 22RV1 cell line. Additionally, the knockdown of DUXAP10 could remarkably inhibit the proliferation, migration, and induce apoptosis of prostate cancer cells, and significantly increase the number of G0/G1 cells in PC3 and DU145 cell lines. Moreover, DUXAP10 could promote the development of prostate cancer by regulating the process of epithelial-mesenchymal transition (EMT). CONCLUSIONS: The findings of this study suggested that the down-regulation of DUXAP10 expression suppressed the progression of prostate cancer by inhibiting cell proliferation, migration and promote cell apoptosis.

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OBJECTIVE: The aim of this study was to investigate the effect of microRNA-539-3p (miR-539-3p) on the development of epithelial ovarian cancer (EOC), and to explore the possible underlying mechanism. PATIENTS AND METHODS: A total of 40 paired EOC tissues and adjacent normal ovarian tissues were surgically resected in Hanchuan People's Hospital. Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) was used to detect the expression of miR-539-3p in EOC tissues and cell lines. Targeted regulatory mechanism of miR-539-3p on SPARC-like protein 1 (SPARCL1) was identified by luciferase reporter and Western blot assays. Furthermore, the effects of miR-539-3p/SPARCL1 axis on the malignant behaviors of EOC cells, including proliferation, invasion and migration abilities, were confirmed by cell counting kit-8 (CCK-8), transwell and scratch wound assays. RESULTS: QRT-PCR showed that the expression of miR-539-3p was significantly up-regulated in EOC tissues and cell lines. SPARCL1 was a direct target of miR-539-3p in EOC cells. Overexpression of miR-539-3p significantly promoted the proliferation, migration and invasion of SKOV3 cells. Furthermore, co-transfection of miR-539-3p inhibitor and si-SPARCL1 could remarkably restore the migration and invasion abilities of SKOV3 cells. CONCLUSIONS: MiR-539-3p acted as an oncogene in EOC by targeting SPARCL1. MiR-539-3p/SPARCL1 axis, as a target for the treatment of EOC, might become a feasible and new method of tumor treatment.

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Objective: To test the effect of metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) and/or osimertinib on the proliferation and apoptosis of HCC827 cells, and explore the potential mechanism of MALAT1 induced resistance to osimertinib. Methods: We transfected HCC827 cells with LV-vector or LV-over/MALAT1. Stable transfected cells (HCC827/Vector, HCC827/MALAT1) were selected by adding puromycin. HCC827/MALAT1 cells were further transfected with the shRNA-negative control (NC) or shRNA-human epidermal growth factor receptor 3 (ERBB3) plasmid. The effects of overexpression of MALAT1, knockdown of ERBB3 and/or osimertinib on the proliferation of HCC827 cells were evaluated by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H tetrazolium bromide (MTT) assay. Cell apoptosis induced by MALAT1 overexpression, knockdown of ERBB3 and/or osimertinib treatment were analyzed by flow cytometry analysis. The expressions of EGFR and ERBB3 signal pathway related proteins in HCC827 cells treated with overexpression of MALAT1, knockdown of ERBB3 and/or osimertinib treatment were detected by western blot. Results: The MTT assay showed that sensitivity to osimertinib of HCC827/MALAT1 cells were significantly repressed. The 50% inhibitive concentration (IC(50)) of osimertinib >4 000 nmol/L in HCC827/MALAT1 cells. However, knockdown of ERBB3 facilitated the anti-proliferation effect of osimertinib, and the IC(50) of osimertinib in shRNA-ERBB3 cells was (17.27±3.21) nmol/L. The results of flow cytometry analysis showed that the apoptotic rate of HCC827/MALAT1 cells induced by 10 nmol/L osimertinib was (8.38±0.92)%, significantly lower than (27.17±5.83)% of knockdown of ERBB3 (P<0.01). Western blotting showed that the expression of p-ERBB3, p-AKT and p-extracellular regulated protein kinases (ERK) in HCC827/MALAT1 cells was markedly up-regulated, while the expression of p-epithelial growth factor receptor (EGFR) was inhibited. The expressions of p-ERBB3, p-AKT and p-ERK were marginally affected by osimertinb. However, osimertinib downregulated the expressions of p-EGFR, p-ERBB3, p-AKT and p-ERK in ERBB3 deleted cells. Conclusions: MALAT1 confers resistance to osimertinb in HCC827 cells by activating of the ERBB3/PI3K/AKT and ERBB3/MAPK/ERK signaling pathways.

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It has been hypothesised that intense metabolism of nectar-inhabiting yeasts (NIY) may change nectar chemistry, including volatile profile, which may affect pollinator foraging behaviours and consequently plant fitness. However, empirical evidence for the plant-microbe-pollinator interactions remains little known. To test this hypothesis, we use a bumblebee-pollinated vine Clematis akebioides endemic to southwest China as an experimental model plant. To quantify the incidence and density of Metschnikowia reukaufii, a cosmopolitan NIY in floral nectar, a combination of yeast cultivation and microscopic cell-counting method was used. To examine the effects of NIY on plant-pollinator interactions, we used real flowers filled with artificial nectar with or without yeast cells. Then the volatile metabolites produced in the yeast-inoculated nectar were analysed with coupled gas chromatography and mass spectrometry (GC-MS). On average 79.3% of the C. akebioides flowers harboured M. reukaufii, and cell density of NIY was high to 7.4 × 104 cells mm-3 . In the field population, the presence of NIY in flowers of C. akebioides increased bumblebee (Bombus friseanus) pollinator visitation rate and consequently seed set per flower. A variety of fatty acid derivatives produced by M. reukaufii may be responsible for the above beneficial interactions. The volatiles produced by the metabolism of M. reukaufii may serve as an honest signal to attract bumblebee pollinators and indirectly promote the female reproductive fitness of C. akebioides, forming a potentially tripartite plant-microbe-pollinator mutualism.

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OBJECTIVE: The aim of this study was to investigate the role of long non-coding RNA (lncRNA) TCL6 in early abortion and to explore its underlying mechanism. PATIENTS AND METHODS: The expression levels of lncRNA-TCL6 and epidermal growth factor receptor (EGFR) in placental tissues of normal pregnancy, threatened abortion pregnancy, spontaneous abortion pregnancy, and induced abortion pregnancy were detected by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR), respectively. Trophoblast cells were transfected with siRNA to knock-down lncRNA-TCL6. Cell viability of trophoblast cells was detected by cell counting kit-8 (CCK-8) assay. The protein expression levels of EGFR, extracellular regulated protein kinases (ERK) and protein kinase B (AKT) in trophoblast cells after lncRNA-TCL6 knockdown were detected by Western blot. Rescue experiments were performed to investigate the relationship between EGFR and lncRNA-TCL6. RESULTS: The expression of lncRNA-TCL6 in placenta tissues of threatened abortion pregnancy was significantly higher than that of normal pregnancy. Meanwhile, the expression of lncRNA-TCL6 in placenta tissues of spontaneous abortion pregnancy was also markedly higher than induced abortion pregnancy. However, the expression of EGFR showed an opposite trend. After knockdown of lncRNA-TCL6 in trophoblast cells, the protein expression levels of EGFR, ERK, and AKT were significantly increased when compared with those of the control group. CCK-8 assay indicated that cell viability was remarkably increased after knockdown of lncRNA-TCL6, which could be reversed by EGFR knockdown. CONCLUSIONS: Compared with normal pregnancy, lncRNA-TCL6 was highly expressed in placental tissues of threatened abortion pregnancy. Moreover, the expression of lncRNA-TCL6 in placenta tissues of spontaneous abortion pregnancy was significantly higher than induced abortion pregnancy. Knockdown of lncRNA-TCL6 promoted the proliferation of trophoblast cells and inhibited the abortion via the EGFR signaling pathway.

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The pollination efficiency hypothesis has long been proposed as an explanation for interspecific variation in pollen-ovule (P:O) ratios. However, no empirical study on P:O ratios has directly and quantitatively measured pollen transfer efficiency (PE). Here, we use a PE index, defined as the proportion of pollen grains removed from anthers that are subsequently deposited on conspecific stigmas, as a direct and quantitative measure of PE. We investigated P:O ratios, pollen removal and pollen deposition in 26 plant species in an alpine meadow, over three consecutive years. Our community survey showed that nearly 5% of removed pollen was successfully deposited on conspecific stigmas. The PE index ranged from 0.01% up to 78.56% among species, and correlated negatively with the P:O ratio across years. This correlation was not changed by controlling for phylogenetic relationships among species, suggesting that the interspecific variation in P:O ratios can be attributed to the probability of pollen grains reaching a stigma. The results indicate that the pollination efficiency hypothesis can help to explain interspecific variation in P:O ratios.

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