Knockdown of linc-POU3F3 suppresses the proliferation, apoptosis, and migration resistance of colorectal cancer

作者: Ti-Dong Shan , Ji-Hao Xu , Tao Yu , Jie-Yao Li , Lin-Na Zhao

DOI: 10.18632/ONCOTARGET.5830

关键词: Gene knockdownCancer researchAutophagyBiologyImmunologySignal transductionCell cycleCyclin D1Epithelial–mesenchymal transitionIntrinsic apoptosisCell growth

摘要: Long intergenic noncoding RNAs (lincRNAs) play important roles in regulating the biological functions and underlying molecular mechanisms of colorectal cancer (CRC). Here, we investigated association linc-POU3F3 prognosis CRC. We demonstrated that was overexpressed CRC tissues positively correlated with tumor grade N stage. Inhibition resulted inhibition cell proliferation G1 cycle arrest, which mediated by cyclin D1, CDK4, p18, Rb, phosphorylated Rb. induced apoptosis, suppressed migration invasion LOVO SW480 lines. This also increased expressions epithelial markers decreased mesenchymal markers, thus inhibiting epithelial-mesenchymal transition. The following knockdown were an BMP signal. Furthermore, autophagy enhanced knockdown, suggesting involvement apoptosis. Collectively, might be crucial pro-proliferation, anti-apoptosis, metastasis cells cycle, intrinsic signaling autophagy. Thus, is a potential therapeutic target novel biomarker for

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