Effect of long non-coding RNA SNHG5 on epithelial-mesenchymal transition and tumor stem cell proliferation
- Author:
Ya-Rui LI
1
Author Information
- Publication Type:Journal Article
- Keywords: Cancer stem cell; Epithelial-mesenchymal transition (EMT); Hepatocellular carcinoma; Long non-coding RNA SNHG5
- From: Journal of Xi'an Jiaotong University(Medical Sciences) 2019;40(6):882-887
- CountryChina
- Language:Chinese
- Abstract: Objective: To investigate the expression of small nucleolar RNA host gene 5 (SNHG5) in hepatocellular carcinoma (HCC) and its effect on epithelial-mesenchymal transition (EMT) and tumor stem cell proliferation. Methods: The expression of SNHG5 gene was detected by qRT-PCR in 48 cases of HCC tissues and corresponding adjacent tissues. The results and clinical pathological parameters were analyzed. The SNHG5 knockdown lentivirus was constructed and transfected into HCC cell lines, and the efficiency was verified by qRT-PCR. The cell invasion and migration abilities were detected by Transwell test; the formation and proliferation of HCC stem cells were detected by stem cell glomeration test. The expressions of EMT and stem cell-related genes mRNA and protein were detected by qRT-PCR and Western blot. Results: In 48 HCC patients, the expression of SNHG5 was significantly higher in HCC than in adjacent normal tissue. The high expression of SNHG5 was associated with tumor size, HBV infection, pathological differentiation type and clinical stage of HCC (P<0.05). At the cellular level, knockdown of SNHG5 inhibited the invasion and migration of HCC lines HepG2 and Huh7 and the number and diameter of cancer stem cells (CSCs). The expression of E-cadherin was significantly increased in the SNHG5 knockdown group while the expressions of N-cadherin and stem cell-associated proteins OCT4 and SOX2 were significantly reduced (P<0.05). Conclusion: SNHG5 is highly expressed in HCC. Knockdown of SNHG5 inhibits the invasion and migration of HCC cells and the proliferation of CSCs. The mechanism may be related to the knockdown of SNHG5 to promote the reversal of HCC cell EMT and reduce the characteristics of HCC cancer stem cells.
