scholarly journals Silencing of microRNA ‐3175 represses cell proliferation and invasion in prostate cancer by targeting the potential tumor‐suppressor SCN4B

Author(s):  
He Huang ◽  
Xiao‐Yan Qing ◽  
Qiong Zhou ◽  
Han‐Dan Li ◽  
Zhu‐Yun Hu
2021 ◽  
pp. 1-9
Author(s):  
Yuxin Li ◽  
Xiaohong Zhuang ◽  
Li Zhuang ◽  
Hongjian Liu

This paper aimed at investigating AS1 expression in prostate cancer (PCa) and its effects on the proliferation and invasion of prostate cancer cells (PCCs). The prostate tissues and the matched adjacent normal prostate tissues excised and preserved during radical prostatectomy in our hospital were collected. The LncRNA NCK1-AS1 expression was detected. PCa patients were followed up for three years to analyze their prognosis. The correlation of LncRNA NCK1-AS1 expression with clinicopathological features was analyzed. Human normal prostate cells and human PCCs were selected, in which LncRNA NCK1-AS1 expression was tested to screen and then transfect the cells. Cell proliferation, invasion and migration were detected. Cell cycles and apoptosis were analyzed. Compared with the adjacent normal tissues, LncRNA NCK1-AS1 was highly expressed in the prostate cancer tissues. Its expression was remarkably different in those with different stages of TNM and with lymphatic metastasis or not. The prognosis of patients with high LncRNA NCK1-AS1 expression was remarkably poorer than that of those with low expression. Compared with the human normal prostate cells, LncRNA NCK1-AS1 expression in the human PCCs remarkably rose, with the greatest difference in 22Rv1 cells. Compared with the Blank group, cell proliferation and the number of plate cloned cells remarkably reduced in the sh-NCK1-AS1 group. Additionally, in this group, the number of invasive and migratory cells remarkably reduced; the expression of invasion-related protein E-cadherin remarkably rose but that of MMP-2 remarkably reduced; cell cycles were arrested and the expression of cycle-related proteins (CDK4, CDK6, cyclin D1) remarkably reduced; the apoptotic rate and the expression of apoptosis-related protein Bax remarkably rose. LncRNA NCK1-AS1 is highly expressed in PCa, so its down-regulation can inhibit PCCs from proliferating and reduce the number of invasive cells.


2020 ◽  
Author(s):  
Xing Zeng ◽  
Zhiquan Hu ◽  
Yuanqing Shen ◽  
Xian Wei ◽  
Jiahua Gan ◽  
...  

Abstract BackgroundAccumulating evidence indicates miR-5195-3p exerts tumor suppressive role in several tumors. However, there is limited research on the clinical significance and biological function of miR-5195-3p in prostate cancer (PCa).MethodsExpression levels of miR-5195-3p and Cyclin L1 (CCNL1) were determined using quantitative real-time PCR. The clinical significance of miR-5195-3p in PCa patients was evaluated using Kaplan-Meier survival analysis and Cox regression models. Cell proliferation and cell cycle distribution were measured by CCK-8 assay and flow cytometry, respectively. The association between miR-5195-3p and CCNL1 was analyzed by luciferase reporter assay.ResultsMiR-5195-3p expression levels were significantly downregulated in 69 paired PCa tissues compared with matched adjacent normal tissues. The decreased miR-5195-3p expression was associated with Gleason score and TNM stage, as well as worse survival prognosis. The in vitro experiments showed that miR-5195-3p overexpression suppressed the proliferation and cell cycle G1/S transition in PC-3 and DU145 cells. Elevated miR-5195-3p abundance was also demonstrated to impair tumor formation in vivo using PC-3 xenografts. Mechanistically, Cyclin L1 (CCNL1) was a direct target of miR-5195-3p in PCa cells, which was inversely correlated with miR-5195-3p in PCa tissues. Importantly, CCNL1 knockdown imitated, while overexpression reversed the effects of miR-5195-3p overexpression on PCa cell proliferation and cell cycle G1/S transition.ConclusionsOur data suggests that miR-5195-3p functions as a tumor suppressor via downregulating G1/S related CCNL1 expression in PCa.


2020 ◽  
Vol 10 ◽  
Author(s):  
Zhao Chen ◽  
Xin Yan ◽  
Guo-Wei Du ◽  
Kurerban Tuoheti ◽  
Xiao-Jie Bai ◽  
...  

2017 ◽  
Vol 41 (2) ◽  
pp. 635-644 ◽  
Author(s):  
Jian Xu ◽  
Rui Zhang ◽  
Jian Zhao

Background/Aims: The novel long noncoding RNA (lncRNA) tumor suppressor candidate 7 (TUSC7) has been reported as a potential tumor suppressor, while the functional role of TUSC7 is still unknown in colorectal cancer (CRC). Here, we characterized TUSC7 expression profile in CRC patients and investigated its biological function and potential molecular mechanism. Methods: RNA isolation, qRT-PCR, cell counter kit-8 assay, cell cycle assay, EdU assay, and western blot were performed. Statistical analyses were performed using SPSS 18.0 software and p value < 0.05 was considered as statistically significant. Results: In a cohort of CRC patients, we found TUSC7 was significantly downregulated in CRC tissues compared with adjacent non-tumor tissues (P < 0.01). Patients with high expression of TUSC7 had better survival than those with low expression of TUSC7 (HR = 0.342, 95% CI: 0.120-0.972, P = 0.044). Cell count kit 8 and EdU assays showed that ectopic expression of TUSC7 in HCT116 and SW480 cells significantly inhibited cell proliferation rate. After silence of TUSC7 with small interfering RNA, cell proliferation rate increased. Flow cytometry analyses revealed cycles were arrested at G1 phase after TUSC7 overexpression. We found there were 2 binding sites of miR-211-3p within the sequence of TUSC7 and TUSC7 expression level was negatively correlated with miR-211-3p. TUSC7 overexpression increased the expression level of CDK6, which is a downstream target of miR-211-3p, in both RNA and protein level. Furthermore, luciferase reporter assay indicated that TUSC7 could sponge miR-211-3p. Conclusion: To summary, we demonstrated that TUSC7 is a potential tumor suppressor in CRC, and TUSC7 could inhibit CRC cell proliferation by completely sponging miR-211-3p.


FEBS Letters ◽  
2006 ◽  
Vol 580 (5) ◽  
pp. 1205-1214 ◽  
Author(s):  
Benyam Asefa ◽  
Jonathan M. Dermott ◽  
Philipp Kaldis ◽  
Karen Stefanisko ◽  
David J. Garfinkel ◽  
...  

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