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Endometrial cancer is one of the chief culprits threatening women's lives. Although numerous epidemiological experiments have been carried out into the aetiology of endometrial cancer, the cause of the disease has been unclear up to now. In recent years, PTPN18, a member of the protein tyrosine phosphatases (PTP) family predicted to be tumour suppressors or oncogenes, has been confirmed to participate in the occurrence and progression of many cancers. Few studies, however, have explained the role in the endometrial cancer. So, it caught our attention to explore if PTPN18 participates in and plays a regulatory role in the proliferation, apoptosis, and metastasis of endometrial cancer. In our results, we found that PTPN18 was overexpressed in endometrial cancer tissue compared to paracancerous tissue by immunohistochemistry. Not only that, silencing of PTPN18 in endometrial cancer cell lines (HEC‐1‐A and HEC‐1‐B) can significantly impair proliferation detected by CCK8 assay and flow cytometry (FCM) analyses and inhibit the metastasis of endometrial cancer cells shown by the scratch test and the Transwell experiment. PTPN18 knockdown can promote the apoptosis of endometrial cancer. In addition, nude mice tumour formation assay confirmed the results in vivo. Although the exact function of PTPN18 in endometrial cancer is unclear, the targeted therapy drugs enhancing PTPN18 may be considered in the future treatment of endometrial carcinoma. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) are often abnormally expressed in human cancers to act as either oncogenes or tumor suppressor genes. MiRNA-501 (miR-501) has been found to be abnormally expressed in certain types of cancer, but its expression and biological role in hemangioma remain to be fully elucidated. In this study, the expression of miR-501 in hemangioma cell lines was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). The TargetScan algorithm, luciferase activity reporter assay, and Western blot analysis were conducted to validate homeobox D10 ( HOXD10 ) as a direct target of miR-501. The results revealed that miR-501 expression was upregulated in hemangioma cell lines. Downregulation of miR-501 inhibited hemangioma cell proliferation, cell cycle progression, colony formation, migration, and invasion in vitro . Bioinformatics analysis indicated that HOXD10 was a putative target of miR-501. In addition, in a luciferase reporter system, it was confirmed that HOXD10 is a direct target of miR-501. It was also demonstrated HOXD10 downregulation reversed the effects of the miR-501 inhibitor on hemangioma cell activities. These findings indicated that miR-501 targeted HOXD10 to promote hemangioma cell processes, suggesting that miR-501 has an oncogenic role in the pathogenesis of hemangioma., Competing Interests: None.

Objective: The study aimed to explore the association between three miRNAs (miR-100-5p, miR-199a-3p and miR-199b-5p) and mTOR induced autophagy in EEC cells. The expression of three miRNAs and autophagy-related genes Beclin1 and LC3 in Ishikawa and KLE cells were detected., Methods: The effects of three miRNAs on proliferation and apoptosis in EEC cells were analyzed in KLE and ISK cells transfected with miR-100-5p, miR-199a-3p and miR-199b-5p mimics and inhibitors. Quantitative real-time polymerase chain reaction (qRT-PCR), CCK-8 method, flow cytometry and luciferase reporter assay were used to assess the effects of three miRNAs on cell viability, proliferation, apoptosis, and autophagy., Results: We found an increased expression of Beclin1 and LC3 in Ishikawa and KLE cells transfected by miR-100-5p, miR-199a-3p and miR-199b-5p mimics compared with NC ( P <0.05). Additionally, Ishikawa and KLE cells transfected with miR-100-5p, miR-199a-3p and miR-199b-5p mimics grew more slowly than mock and mimics control ( P <0.05); we also found an increased apoptosis incidence of Ishikawa cell transfected with miR-100-5p, miR-199a-3p and miR-199b-5p mimics ( P <0.05). Finally, luciferase reporter results showed miR-100-5p, miR-199a-3p and miR-199b-5p were all down-regulated the luciferase activity in cells transfected with miRNA mimics compared with mock. All results suggested that miR-100-5p, miR-199a-3p and miR-199b-5p may induce the autophagic death of EEC cell through targeting mTOR., Conclusions: Our results suggested that miR-100-5p, miR-199a-3p and miR-199b-5p may induce the autophagic death of EEC cell through targeting mTOR., Competing Interests: None., (IJCEP Copyright © 2017.)