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长链非编码RNA-POU3F3的敲低可抑制结直肠癌的增殖、凋亡及迁移抗性。

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

作者信息

Shan Ti-Dong, Xu Ji-Hao, Yu Tao, Li Jie-Yao, Zhao Lin-Na, Ouyang Hui, Luo Su, Lu Xi-Ji, Huang Can-Ze, Lan Qiu-Shen, Zhong Wa, Chen Qi-Kui

机构信息

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.

Department of Gastroenterology, the First Affiliated Hospital, Guangzhou University of Traditional Chinese Medicine, Guangzhou, Guangdong 510504, People's Republic of China.

出版信息

Oncotarget. 2016 Jan 5;7(1):961-75. doi: 10.18632/oncotarget.5830.

DOI:10.18632/oncotarget.5830
PMID:26510906
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4808045/
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.

摘要

长链基因间非编码RNA（lincRNAs）在调节结直肠癌（CRC）的生物学功能和潜在分子机制中发挥着重要作用。在此，我们研究了linc-POU3F3与CRC预后的相关性。我们证明linc-POU3F3在CRC组织中过表达，且与肿瘤分级和N分期呈正相关。抑制linc-POU3F3导致细胞增殖受到抑制和G1期细胞周期阻滞，这是由细胞周期蛋白D1、细胞周期蛋白依赖性激酶4、p18、视网膜母细胞瘤蛋白（Rb）和磷酸化Rb介导的。抑制linc-POU3F3可诱导细胞凋亡，并抑制LOVO和SW480细胞系的迁移和侵袭。这种抑制还增加了上皮标志物的表达，降低了间充质标志物的表达，从而抑制了癌症上皮-间质转化。linc-POU3F3敲低后迁移和侵袭能力的降低是由骨形态发生蛋白（BMP）信号增强介导的。此外，linc-POU3F3敲低可增强自噬，提示自噬参与了诱导的细胞凋亡。总体而言，linc-POU3F3可能通过调节细胞周期、内源性凋亡、BMP信号和自噬在LOVO和SW480细胞的促增殖、抗凋亡和转移中起关键作用。因此，linc-POU3F3是CRC潜在的治疗靶点和新型分子生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a75/4808045/5aa4444f05d1/oncotarget-07-0961-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a75/4808045/c8344744876d/oncotarget-07-0961-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a75/4808045/5aa4444f05d1/oncotarget-07-0961-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a75/4808045/a9799b8adbad/oncotarget-07-0961-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a75/4808045/aec62363e24e/oncotarget-07-0961-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a75/4808045/2c63e56428f9/oncotarget-07-0961-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a75/4808045/ea6f804a1aa2/oncotarget-07-0961-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a75/4808045/7aed0a9d2313/oncotarget-07-0961-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a75/4808045/c8344744876d/oncotarget-07-0961-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a75/4808045/5aa4444f05d1/oncotarget-07-0961-g007.jpg

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