目的： 探讨lncRNA SNHG10在结直肠癌组织和细胞中的表达情况及其对结直肠癌细胞侵袭和迁移的影响与可能的机制。 方法： 收集2018年1月至2019年12月在河南省人民医院行根治性结直肠癌切除术的78例患者的癌组织及对应癌旁组织标本，采用qPCR法检测结直肠癌组织、结直肠癌细胞（SW480、SW620、HT-29和LoVo）及人正常结直肠黏膜细胞FHC中lncRNA SNHG10和miR-532-3p的表达水平，并分析其与结直肠癌患者临床病理特征的关系及在组织中表达的相关性。采用双荧光素酶报告基因实验验证lncRNA SNHG10和miR-532-3p间的靶向关系。向SW620细胞中转染si-SNHG10或miR-532-3p mimic或共转染si-SNHG10+miR-532-3p inhibitor，采用Transwell实验检测其侵袭和迁移能力的改变，采用WB法检测E-cadherin，N-cadherin和vimentin蛋白表达水平变化。 结果： SNHG10 在结直肠癌组织和细胞中呈高表达（P<0.05 或 P<0.01），其表达水平与TNM分期和远处转移有关（均P<0.05）；miR-532-3p在结直肠癌组织和细胞中呈低表达，其表达水平与TNM分期、淋巴结转移和远处转移有关（P<0.05或P<0.01），SNHG10和miR-532-3p在结直肠癌组织中的表达呈负相关（r=-0.225, P=0.048）。双荧光素酶报告基因实验证实SNHG10靶向调节miR-532-3p的表达。下调 SNHG10 或上调 miR-532-3p 的表达后，SW620 细胞的侵袭和迁移能力显著降低（P<0.01），E-cadherin蛋白表达水平升高（P<0.05）、N-cadherin和vimentin蛋白表达水平降低（均P<0.05）。抑制miR-532-3p表达后，敲低lncRNA SNHG10表达对结直肠癌细胞侵袭和迁移的抑制作用被逆转（均P<0.05）。 结论： lncRNA SNHG10在结直肠癌中高表达并与TNM分期和远处转移相关，lncRNASNHG10靶向调控miR-532-3p表达并通过EMT途径影响结直肠癌细胞的侵袭和转移。

Objective: To investigate the expression of long non-coding RNA (lncRNA) small nucleolar RNA host gene 10 (SNHG10) in colorectal cancer tissues and cells and its effect on the invasion and migration of colorectal cancer cells and the underlying mechanism. Methods: From January 2018 to December 2019, 78 pairs of colorectal cancer tissue and para-cancerous tissues from the patients who had radical colorectal cancer resection in Henan Provincial People's Hospital were collected. Quantitative PCR (qPCR) was performed to quantify the levels of lncRNA SNHG10 and miR-532-3p in colorectal cancer tissues, colorectal cancer cell lines (SW480, SW620, HT-29 and LoVo) and human normal colorectal mucosal FHC cells; and their correlations with the clinicopathological features of colorectal cancer patients were further analyzed. Dual-luciferase reporter gene assay was used to validate the targeted relationship between lncRNA SNHG10 and miR-532-3p. After transfection with si-SNHG10 or miR-532-3p mimic or co-transfection of si-SNHG10 and miR-532-3p inhibitor, the invasion and migration of SW620 cells were detected by Transwell assay, and the protein expression of E-cadherin, N-cadherin and vimentin were detected by WB. Results: SNHG10 was highly expressed in colorectal cancer tissues and cells (all P<0.05), and its expression was related to TNM stage and distant metastasis (all P<0.05). miR-532-3p was lowly expressed in colorectal cancer tissues and cells, and its expression was correlated with TNM stage, lymphonode metastasis and distant metastasis (all P<0.05). The expression of SNHG10 and miR-532-3p in colorectal cancer tissues was negatively correlated (r=-0.225, P=0.048). Dual-luciferase reporter gene assay confirmed that SNHG10 targetedly regulated miR-532-3p. Both down-regulation of SNHG10 and up-regulation of miR-532-3p significantly inhibited the invasion and migration of SW620 cells (all P<0.05), up-regulated the expression of E-cadherin (P<0.05), while down-regulated the expression of N-cadherin and vimentin (all P<0.05). After transfection with miR-532-3p inhibitor, the inhibitory effect of knocking down the expression of lncRNA SNHG10 on the invasion and migration of colorectal cancer cells was reversed (all P<0.05). Conclusions: LncRNA SNHG10 is highly expressed in colorectal cancer and is associated with TNM stage and distant metastasis. LncRNA SNHG10 affects the invasion and metastasis of colorectal cancer cells by targeting miR-532-3p and regulating EMT.

R735.3；R730.2

国家自然科学基金青年基金（No. 81802094）