Objective: To investigate the effects of lncRNA SNHG11 on proliferation, migration, invasion and apoptosis of colorectal cancer cancer cells and possible mechanisms. Methods: qRT-PCR was performed to detect the expression level of lncRNA SNHG11 in colorectal cancer tissues and its related cell lines. The correlation between SNHG11 expression and clinical prognosis of patients was assessed by bioinformatics techniques. Cultured CRC cell lines were transfected with shCtrl (shCtrl group), shSNHG11#1 (shSNHG11#1 group), shSNHG11#2 (shSNHG11#2 group), Control cDNA (Control cDNA group), and SNHG11 cDNA (SNHG11 cDNA), respectively. Thiazolyl blue (MTT), clone formation assay, Transwell assay, cell scratch assay, and flow cytometry were used to detect the proliferation, migration, invasion, and apoptosis of CRC cells in each group. Western protein blotting was used to detect the expression of relevant proteins in each group, and the effect of lncRNA SNHG11 knockdown on the growth of tumour cells in vivo was analysed by nude mice tumouring assay. Phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signalling pathway inhibitor LY294002 was used for rescue experiments. Results: The expression of lncRNA SNHG11 was significantly higher in colorectal cancer cells and tissues than in normal tissues (P<0.05). Survival analysis showed that the expression level of SNHG11 was not statistically associated with CRC survival (P>0.05). shSNHG11#2 group compared with shCtrl group. MTT OD490/570 values decreased, the number of CRC cell clones decreased, the number of Transwell cells decreased, the area of cell scratch decreased, and the apoptosis rate increased (P<0.05). The mesenchymal markers matrix metalloproteinase (MMP9), N-cadherin and vimentin were significantly reduced, and the expression of the epithelial marker E-cadherin was upregulated. The expression of anti-apoptotic proteins Bcl-2 and Bcl-xl was decreased, and the expression of pro-apoptotic protein Bax was increased (P<0.05).In vivo experiments showed that lncRNA SNHG11 knockdown inhibited the growth of colorectal cancer cells, and the expression of Ki67 was reduced in tumours (P<0.05). LncRNA SNHG11 knockdown inhibited the expression of p-PI3K, p-Akt and p-mTOR.The PI3K/Akt/mTOR signaling pathway inhibitor LY294002 was able to restore the malignant cytological progression of colorectal cancer cells induced by the overexpression of lncRNA SNHG11. Conclusions: LncRNA SNHG11 is highly expressed in colorectal cancer. lncRNA SNHG11 can promote the malignant progression of colorectal cancer cells by regulating the PI3K/Akt/mTOR signaling pathway, and this finding provides a new theoretical basis for targeted therapy of colorectal cancer.
目的： 探讨长链非编码（lnc）RNA SNHG11对结直肠癌（CRC）细胞增殖、迁移、侵袭和凋亡的影响及可能的作用机制。 方法： 采用实时定量聚合酶链反应（qRT-PCR）检测lncRNA SNHG11在CRC患者CRC组织及其相关细胞系中的表达水平。通过生物信息学技术评估SNHG11表达与患者临床预后的相关性。培养CRC细胞株分别转染shCtrl（shCtrl组）、shSNHG11#1（shSNHG11#1组）、shSNHG11#2（shSNHG11#2组）、Control cDNA（Control cDNA组）、SNHG11 cDNA（SNHG11 cDNA）。噻唑蓝（MTT）、克隆形成实验、Transwell实验、细胞划痕实验、流式细胞术检测各组CRC细胞增殖、迁移、侵袭和凋亡。Western印迹法检测各组相关蛋白表达，并通过裸鼠成瘤实验分析lncRNA SNHG11敲低对肿瘤细胞体内生长的影响。磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（Akt）/哺乳动物雷帕霉素靶蛋白（mTOR）信号通路抑制剂LY294002用于挽救实验。 结果： lncRNA SNHG11在CRC细胞和组织中的表达明显高于正常组织，差异有统计学意义（P<0.05）。生存分析显示，SNHG11表达水平与CRC的生存无统计学意义（P>0.05）。shSNHG11#2组与shCtrl组相比，MTT OD490/570值下降，CRC细胞克隆数目减少，Transwell细胞数目减少，细胞划痕面积减小，细胞凋亡率升高（P<0.05）。间质标志物基质金属蛋白酶（MMP9），N-钙黏蛋白（N-cadherin）和波形蛋白（Vimentin）均显著降低，上皮标志物E-钙黏蛋白（E-cadherin）表达上调。抗凋亡蛋白Bcl-2和Bcl-xl表达降低，促凋亡蛋白Bax表达增加（P<0.05）。体内试验表明，lncRNA SNHG11敲低可抑制CRC细胞生长，瘤体内Ki67表达减低（P<0.05）。lncRNA SNHG11敲低可抑制p-PI3K、p-Akt和p-mTOR的表达，使用PI3K/Akt/mTOR信号通路抑制剂LY294002能够恢复lncRNA SNHG11过表达引起的CRC细胞恶性细胞学进程。 结论： lncRNA SNHG11在CRC中高表达，lncRNA SNHG11可通过调节PI3K/Akt/mTOR信号通路促进CRC细胞恶性进展。.