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首页> 外文期刊>Journal of cellular physiology. >Long intergenic noncoding RNA 00908 promotes proliferation and inhibits apoptosis of colorectal cancer cells by regulating KLF5 expression
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Long intergenic noncoding RNA 00908 promotes proliferation and inhibits apoptosis of colorectal cancer cells by regulating KLF5 expression

机译：00908促进长基因间的非编码RNA增殖和抑制细胞凋亡结直肠癌细胞通过调节KLF5表达式

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摘要

Long intergenic noncoding RNAs (lincRNAs) play a vital role in the occurrence and progression of cancer. The mechanism of lincRNAs in colorectal cancer (CRC) has not been fully elucidated. In this context, an integrated comparative long noncoding RNA (lncRNA) microarray technology was used to determine the expression profile of lncRNAs in CRC. The roles of LINC00908 are unclear. We found that LINC00908 was significantly upregulated in CRC. Inhibition of LINC00908 resulted in reduced cell proliferation and G1 cell cycle arrest, which was mediated by cyclin D1, cyclin-dependent kinase 4, and phosphorylated retinoblastoma. Moreover, inhibition of LINC00908-induced apoptosis through the intrinsic apoptosis signaling pathway, as shown by the activation of caspase-9 and caspase-3. Mechanistically, miR-143-3p directly bound to LINC00908. miR-143-3p expression was negatively correlated with LINC00908 expression in CRC tissue. Functional experiments revealed opposing roles for miR-143-3p and LINC00908, suggesting that LINC00908 negatively regulates miR-143-3p. Mechanistically, miR-143-3p directly targets LINC00908. The KLF5 inhibitor ML264 affected proliferation and apoptosis, indicating that LINC00908 may act as a competing endogenous RNA to facilitate the expression of the miR-143-3p target gene KLF5. Thus, LINC00908 has an important proliferative and antiapoptotic role in CRC by regulating the cell cycle and intrinsic apoptosis. LINC00908 could be a potential biomarker and a new therapeutic target for CRC.
机译：长基因间的非编码rna (lincRNAs)扮演发生和发展的至关重要的作用癌症。癌症(CRC)尚未完全阐明。这种情况下,一个集成的比较长非编码RNA (lncRNA)微阵列技术用来确定的表达谱lncRNAs CRC。不清楚。在CRC显著调节。LINC00908导致细胞增殖减少G1细胞周期阻滞,是由细胞周期蛋白D1,细胞周期蛋白依赖性激酶4,磷酸化视网膜母细胞瘤。LINC00908-induced抑制细胞凋亡内在的细胞凋亡信号通路,caspase-9的激活和显示caspase-3。绑定到LINC00908。LINC00908表达呈负相关在结肠组织。对立的角色mir - 143 - 3 p和LINC00908这表明LINC00908负调节mir - 143 - 3 - p。LINC00908目标。增殖和凋亡的影响,表明LINC00908可能作为内生竞争RNA的表达促进mir - 143 - 3 - p KLF5目标基因。一个重要的增殖和凋亡的作用CRC通过调节细胞周期和内在细胞凋亡。生物标志物和CRC的新的治疗目标。

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