Circular RNA circFOXM1 triggers the tumorigenesis of non-small cell lung cancer through miR-132-3p/TMEM14A axis

Farlier studies indicated that circular RNAs(circRNAs)were found in various cancer clls,and circFOXM1 was reported to act as an oncogane in non-small cell lung cancer(NSCLC).However,the function of circFOXM1 in NSCLC remains undear.The epression lewels of genes were measured using quantative real-time polymerase chain reactions(qRT-PCR).Cell prolferation and apoptosis were determined by 3-(4,5 dimethylthiazol-2-yl)-25 dipbenyletrazolium bromide solution(MTT)and flow cytometry assay.The rdative protein expression was assed by westen blot Moreower,transwell assays were employed to examine ell migration and invasion.The targeted relationship was confirmed by dual-luciferase reporter assay.The expression of circFOXMI was up-regulated in NSCIC tissues and cell lines.The depletion of circFOXM1 decreased the prolferation,migration,invasion,and induced cell apoptosis of NSCLC cells.MicroRNA-132-3p(MiR-1323p)was idenified as a target of dircFOXMl.The expression level of miR-132-3p was decrased in NSCLC tssues and cell lines and inversely corrdated with circFOXM1 expression.Furthermore,the efects of drdOXMl down regulation on NSCLC cell progression were abolished by mR-1323p inhibitor.Transmembrane protein 14A(TMEM14A)was verifed as a target gene of miR-132-3p.The efects of circFOXM1 depletion on NSCLC cell proliferation,apoptosis,migration,and invasion were reversed by TMEMI4A overexpression.Our study demonstrated that knodkdown of circFOXM1 suppressed NSCLC progression through rqgulating miR-132-3p/TMEMI4A axis,sugesting the drFOXM/miR-132-3p/TMEM14A axis may serve as the novd target for NSCLC diagnosis and therapy.

Oncogenic miR-19a and miR-19b co-regulate tumor suppressor MTUS1 to promote cell proliferation and migration in lung cancer

MTUS1 （microtubule-associated tumor suppressor 1） has been identified that can function as a tumor sup- pressor gene in many malignant tumors. However, the function and mechanisms underlying the regulation of MTUS1 are unclear. In the present study, we reported that miR-19a and miR-19b （miR-19a/b） promote prolifer- ation and migration of lung cancer cells by targeting MTUS1. First, MTUS1 was proved to function as a tumor suppressor in lung cancer and was linked to cell prolif- eration and migration promotion. Second, an inverse correlation between miR-19a/b expression and MTUS1 mRNA/protein expression was noted in human lung cancer tissues. Third, MTUS1 was appraised as a direct target of miR-19a/b by bioinformatics analysis. Fourth, direct MTUS1 regulation by miR-19a/b in lung cancer cells was experimentally affirmed by cell transfection assay and luciferase reporter assay. Finally, miR-19a/b were shown to cooperatively repress MTUS1 expression and synergistically regulate MTUS1 expression to pro- mote lung cancer cell proliferation and migration. In conclusion, our findings have provided the first cluesregarding the roles of miR-19a/b, which appear to func- tion as oncomirs in lung cancer by downregulating MTUSI.

Effects of miR-200c on the migration and invasion abilities of human prostate cancer Du145 cells and the corresponding mechanism

microRNAs （miRNAs） have played a key role in human tumorigenesis, tumor progression, and metastasis. On the one hand, miRNAs are aberrantly expressed in many types of human cancer; on the other hand, miRNAs can function as tumor suppressors or oncogenes that target many cancer-related genes. This study aimed to investigate the effects of miRNA-200c （miR-200c） on the biological behavior and mechanism of proliferation, migration, and invasion in the prostate cancer cell line Du145. In this study, Du145 cells were transfected with miR-200c mimics or negative control miR-NC by using an X-tremeGENE siRNA transfection reagent. The relative expression of miR-200c was measured by RT-PCR. The proliferation, migration, and invasion abilities of Du145 cells were detected by CCK8 assays, migration assays and invasion assays, respectively. The expressions of ZEB1, E-cadherin, and vimentin were observed by western blot. Results showed that DU145 cells exhibited a high expression of miR-200e compared with immortalized normal prostate epithelial cell RWPE-1. Du145 cells were then transfected with miR-200c mimics and displayed lower abilities of proliferation, migration, and invasion than those transfected with the negative control. The protein levels of ZEB1 and vimentin were expressed at a low extent in Du145 cells, which were transfected with miR-200c mimics; by contrast, E-cadherin was highly expressed. Hence, miR-200c could significantly inhibit the proliferation of the prostate cancer cell line Du145; likewise, miR- 200c could inhibit migration and invasion by epithelial-mesenchymal transition.

COTE-1上调Yap促进非小细胞肺癌细胞增殖和侵袭

目的探讨COTE-1蛋白在非小细胞肺癌中的表达及对肺癌细胞增殖和侵袭的影响。方法免疫组织化学染色检测COTE-1在肺癌组织中的表达;克隆形成实验和Transwell实验检测COTE-1对肺癌细胞增殖和侵袭能力的影响;Western blot检测COTE-1对肺癌细胞YAP和CTGF蛋白表达的影响。结果 COTE-1在非小细胞肺癌组织和细胞系中明显高表达,COTE-1过表达促进肿瘤细胞增殖和侵袭能力,COTE-1过表达上调YAP及靶基因CTGF促进非小细胞肺癌的演进。结论 COTE-1参与调控YAP及靶基因CTGF的表达,可作为一个肺癌的潜在治疗靶点。