Department of Medical Oncology, Shaanxi Provincial People's Hospital, Xi'An, China.
Eur Rev Med Pharmacol Sci. 2018 Oct;22(19):6315-6323. doi: 10.26355/eurrev_201810_16042.
The aim of this study was to explore whether LINC00657 can regulate cell proliferation and invasion by regulating the PI3K/AKT pathway and thus participate in the occurrence of colon cancer.
Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was applied to detect the expression levels of LINC00657 and E-cad in colon cancer tissues and corresponding adjacent tissues obtained from 80 patients, and the correlation was analyzed between LINC00657 expression and clinical information of patients such as prognosis, tumor size, tumor stage, and distant metastasis. The expression of LINC00657 and E-cad in colon cancer cell lines was also examined, and the effect of LINC00657 on tumor cell proliferation was evaluated by cell counting kit-8 (CCK-8) assay and colony formation experiments. Meanwhile, transwell assay was performed to evaluate the influence of LINC00657 and CAPN7 on cell invasive ability. In addition, the effect of LINC00657 on CAPN7 and PI3K/AKT pathway was detected by Western blot assay.
The expression levels of LINC00657 and E-cad in tumor tissues decreased remarkably, especially in patients who occurred distant metastasis. Compared with patients with highly-expressed LINC00657, the patients with lower level of LINC00657 had a worse prognosis and an advanced tumor size and TNM stage. Similarly, LINC00657 and E-cad also showed a decrease in colon cancer cell lines. After overexpression of LINC00657, cell viability and invasive ability decreased remarkably while cell apoptosis rate increased significantly. In addition, high expression of LINC00657 in an in vitro model significantly promoted CAPN7 expression and inhibited activation of PI3K/AKT pathway.
LINC00657 had a low expression in colon cancer tissues, which could accelerate cell proliferation and invasion by activating PI3K/AKT pathway and inhibiting CAPN7 expression.
本研究旨在探讨 LINC00657 是否可以通过调节 PI3K/AKT 通路来调节细胞增殖和侵袭，从而参与结肠癌的发生。
应用实时定量聚合酶链反应(qRT-PCR)检测 80 例结肠癌组织及其相应的癌旁组织中 LINC00657 和 E-cad 的表达水平，并分析 LINC00657 表达与患者预后、肿瘤大小、肿瘤分期、远处转移等临床资料的相关性。检测结肠癌细胞系中 LINC00657 和 E-cad 的表达，并通过细胞计数试剂盒-8(CCK-8)检测和集落形成实验评估 LINC00657 对肿瘤细胞增殖的影响。同时，通过 Transwell 实验评估 LINC00657 和 CAPN7 对细胞侵袭能力的影响。此外，通过 Western blot 检测 LINC00657 对 CAPN7 和 PI3K/AKT 通路的影响。
肿瘤组织中 LINC00657 和 E-cad 的表达水平明显降低，尤其是发生远处转移的患者。与高表达 LINC00657 的患者相比，低水平 LINC00657 的患者预后较差，肿瘤大小和 TNM 分期也较晚。同样，LINC00657 和 E-cad 在结肠癌细胞系中也出现下调。过表达 LINC00657 后，细胞活力和侵袭能力明显降低，而细胞凋亡率显著升高。此外，体外模型中 LINC00657 的高表达显著促进 CAPN7 的表达，抑制 PI3K/AKT 通路的激活。
LINC00657 在结肠癌组织中表达较低，通过激活 PI3K/AKT 通路和抑制 CAPN7 表达，促进细胞增殖和侵袭。
