J Cancer 2020; 11(10):3002-3012. doi:10.7150/jca.40592

Research Paper

Long noncoding RNA SNHG6 promotes proliferation and angiogenesis of cholangiocarcinoma cells through sponging miR-101-3p and activation of E2F8

Huishan Wang1*, Li Wang1*, Lingyu Tang2*, Jing Luo3, Hao ji1, Wen Zhang1, Jian Zhou1, Quanpeng Li4, Lin Miao1,4✉

1. Nanjing Medical University, 101 Longmian Avenue, Jiangning District, Nanjing 211166, Jiangsu Province, China.
2. Taizhou hospital of traditional Chinese medicine, 86 Jichuandong Road, Hailing District, Taizhou 225300, Jiangsu Province, China.
3. Department of Thoracic Surgery, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, China
4. Medical Center for Digestive Diseases, The Second Affiliated Hospital of Nanjing Medical University, 121 Jiangjiayuan, Nanjing 210011, Jiangsu Province, China.
*These authors contributed equally to the work and should be regarded as joint first authors.

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Citation:
Wang H, Wang L, Tang L, Luo J, ji H, Zhang W, Zhou J, Li Q, Miao L. Long noncoding RNA SNHG6 promotes proliferation and angiogenesis of cholangiocarcinoma cells through sponging miR-101-3p and activation of E2F8. J Cancer 2020; 11(10):3002-3012. doi:10.7150/jca.40592. Available from http://www.jcancer.org/v11p3002.htm

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Abstract

Cholangiocarcinoma (CCA) development is an extremely complex process with alterations occurring in numerous genes. SNHG6, a validated lncRNA, has been reported to regulate the expression of multiple tumor-related genes in hepatocellular carcinoma, colorectal cancer and breast cancer. Here, we elucidated the function and possible molecular mechanisms of SNHG6 in human CCA cells. Our results proved that the expression SNHG6 was upregulated in CCA tissues and cell lines. Ectopic expression of SNHG6 promoted cell proliferation, cell cycle progression, migration, and angiogenesis in CCA cells, whereas knockdown of SNHG6 repressed these cellular processes. Further mechanistic studies revealed that SNHG6 could compete with the transcription factor E2F8 to bind with miR-101-3p, thus affecting E2F8 expression. Taken together, these results provided a comprehensive analysis of the role of SNHG6 in CCA cells and offered important clues to understand the key roles of competing endogenous RNA (ceRNA) mechanisms in human cholangiocarcinoma.

Keywords: cholangiocarcinoma, SNHG6, miR-101-3p, E2F8, ceRNA