Journal
JOURNAL OF CANCER
Volume 11, Issue 10, Pages 3002-3012Publisher
IVYSPRING INT PUBL
DOI: 10.7150/jca.40592
Keywords
cholangiocarcinoma; SNHG6; miR-101-3p; E2F8; ceRNA
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Funding
- Project of the Peak of the Six Talents of Jiangsu Province [WSN-018]
- Scientific Research Foundation for Health of Jiangsu Province [H201408]
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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.
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