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

2015; Impact Journals LLC; Volume: 7; Issue: 1 Linguagem: Inglês

10.18632/oncotarget.5830

1949-2553

Ti‐Dong Shan, Jihao Xu, Tao Yu, Jieyao Li, Linna Zhao, Hui Ouyang, Su Luo, Xi-Ji Lu, Can‐Ze Huang, Qiu-Shen Lan, Wa Zhong, Qi‐Kui Chen,

RNA modifications and cancer

// Ti-Dong Shan 1 , Ji-Hao Xu 1 , Tao Yu 1 , Jie-Yao Li 1 , Lin-Na Zhao 3 , Hui Ouyang 1 , Su Luo 1 , Xi-Ji Lu 1 , Can-Ze Huang 1 , Qiu-Shen Lan 2 , Wa Zhong 1 , Qi-Kui Chen 1 1 Department of Gastroenterology and Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, Guangdong 510120, People's Republic of China 2 Department of General Surgery, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, Guangdong 510120, People's Republic of China 3 Department of Gastroenterology, the First Affiliated Hospital, Guangzhou University of Traditional Chinese Medicine, Guangzhou, Guangdong 510504, People's Republic of China Correspondence to: Tao Yu, e-mail: yutao2014@126.com Qi-Kui Chen, e-mail: qikuichen@yahoo.com Keywords: linc-POU3F3, colorectal cancer, proliferation, apoptosis, signal pathway Received: June 18, 2015 Accepted: September 24, 2015 Published: October 15, 2015 ABSTRACT Long intergenic noncoding RNAs (lincRNAs) play important roles in regulating the biological functions and underlying molecular mechanisms of colorectal cancer (CRC). Here, we investigated the association of linc-POU3F3 and prognosis in CRC. We demonstrated that linc-POU3F3 was overexpressed in CRC tissues and positively correlated with tumor grade and N stage. Inhibition of linc-POU3F3 resulted in inhibition of cell proliferation and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, p18, Rb, and phosphorylated Rb. Inhibition of linc-POU3F3 induced apoptosis, and suppressed migration and invasion in LOVO and SW480 cell lines. This inhibition also increased the expressions of epithelial markers and decreased the expressions of mesenchymal markers, thus inhibiting the cancer epithelial-mesenchymal transition. The decreased migration and invasion following linc-POU3F3 knockdown were mediated by an increased BMP signal. Furthermore, autophagy was enhanced by linc-POU3F3 knockdown, suggesting the involvement of autophagy in the induced apoptosis. Collectively, linc-POU3F3 might be crucial in pro-proliferation, anti-apoptosis, and metastasis in LOVO and SW480 cells by regulating the cell cycle, intrinsic apoptosis, BMP signaling and autophagy. Thus, linc-POU3F3 is a potential therapeutic target and novel molecular biomarker for CRC.