lncRNA FLJ26245 regulates the proliferation and migration of prostate cancer PC-3 cells through miR-200a-3p/PTPRG axis / 中国肿瘤生物治疗杂志

@#[摘 要] 目的：探讨lncRNA FLJ26245在前列腺癌组织和细胞中的表达及其对PC-3细胞增殖与迁移能力的影响及其分子机制。方法：选用2017年3月至2019年5月在洛阳中心医院手术切除的52例前列腺癌及相应的癌旁组织标本，以及前列腺细胞系LNCaP、C4-2B、PC-3、DU-145和正常前列腺上皮细胞RWPE-1，用qPCR法检测前列腺癌组织和细胞中FLJ26245的表达水平。分别将FLJ26245 mimic和阴性对照质粒（lncR-NC）转染到PC-3细胞中，用MTT法、细胞划痕愈合实验分别检测细胞的增殖和迁移能力。生物信息学技术预测和双荧光素酶基因报告实验验证FLJ26245与miR-200a-3p、酪氨酸磷酸酶受体G（PTPRG）三者之间的靶向关系。用qPCR和WB法分别检测FLJ26245下游基因及增殖与迁移相关蛋白的表达。结果：FLJ26245在前列腺癌组织和细胞中的表达水平分别显著低于癌旁组织（P<0.01）和RWPE-1细胞（P<0.01或P<0.05），以PC-3细胞中的表达水平为最低（P<0.01）。FLJ26245过表达可明显抑制PC-3细胞的增殖和迁移能力（P<0.05或P<0.01）。FLJ26245可与miR-200a-3p靶向结合，miR-200a-3p可与PTPRG靶向结合（均P<0.01）。FLJ26245过表达的PC-3细胞中miR-200a-3p表达水平显著降低（P<0.01）、PTPRG mRNA和蛋白表达水平均明显升高（均P<0.01），细胞中增殖和迁移相关蛋白cyclin A、CDK2和Twist、N-cadherin均显著降低（均P<0.01）。结论：FLJ26245在前列腺癌组织及细胞中均低表达，其可能通过miR-200a-3p/PTPRG轴调控前列腺癌PC-3细胞的增殖与迁移能力。

Expression of lncRNA GTSE1-AS1 in prostate cancer tissues and its effect on proliferation and invasion of LNCaP cells / 中国肿瘤生物治疗杂志

@#[Abstract] Objective: To explore the expression of long non-coding RNA (lncRNA) GTSE1-AS1 in prostate cancer tissues and the mechanism that affects the proliferation and invasion of LNCaP cells. Methods: From November 2017 to December 2018, 68 pairs of prostate cancer tissue and para-cancerous tissue specimens were resected from prostate cancer patients at the Department of Urology of Luoyang Central Hospital Affiliated to Zhengzhou University; in addition, prostate cancer cell lines LNCaP, PC-3, C4-2B, 22Rv1, DU-145 and normal prostate follicular epithelial RWPE-1 cells were also chosen for this study. qPCR was used to detect the expression level of GTSE1-AS1 in cancer tissues and cell lines. The GTSE1-AS1 over-expression plasmid (experimental group) and negative control plasmid (control group) were respectively transfected into LNCap cells. MTT assay and Transwell chamber method were used to detect the effect of GTSE1-AS1 over-expression on the proliferation and invasion ability of LNCaP cells, respectively. The targeting relationship among GTSE1-AS1 and miR-324-3P as well as FBXW7 (F-frame/WD repeat domain protein 7) was verified by bioinformatics tools and dual-luciferin reporter gene assay. The effect of GTSE1-AS1 over-expression on downstream gene and protein expression was detected by qPCR and WB assay. Results: The expression level of GTSE1-AS1 in prostate cancer tissues was significantly lower than that in para-cancerous tissues (P<0.01), and the expression of GTSE1-AS1 in prostate cancer cell lines was significantly lower than that in RWPE-1 cells (P<0.05 or P<0.01). Over-expression of GTSE1-AS1 significantly inhibited the proliferation and invasion (P<0.05 or P<0.01) of LNCaP cells. Dual-luciferin reporter gene assay confirmed the complementary binding between GTSE1-AS1 and miR-324-3p as well as between miR-324-3p and FBXW7. Over-expression of GTSE1-AS1 significantly reduced the expression of miR-324-3p in LNCaP cells (P<0.01), and promoted the mRNA and protein expressions of FBXW7 (all P<0.01). Conclusion: GTSE1-AS1 is under-expressed in prostate cancer tissues and cell lines. Over-expression of GTSE1-AS1 can inhibit the proliferation and invasion of LNCaP cells, the mechanism of which may be related with the inhibition of miR-324-3p to further promote FBXW7 expression.