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RASAL2 acts as a tumor suppressor in cervical cancer cells

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BIOCELL
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TECH SCIENCE PRESS
DOI: 10.32604/biocell.2023.027308

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RASAL2; Cervical cancer; Knockdown; Silencing; Tumor suppressor

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This study investigated the roles of RASAL2 in cervical cancer (CC). The expression of RASAL2 mRNA and protein in CC tissues, CC cell lines, and normal cervical cells was examined. It was found that RASAL2 expression was significantly down-regulated in CC tissues and cell lines, and low expression was associated with advanced stage and metastasis of CC. Over-expression of RASAL2 inhibited proliferation and metastasis of CC cells, while silencing of RASAL2 expression increased the proliferation, invasion, and migration of CC cells. In conclusion, RASAL2 functions as a tumor suppressor in CC and is down-regulated in CC tissue samples and cell lines.
Background: This study was designed to investigate the roles of RASAL2 in cervical cancer (CC). Methods: Fifty-four CC tissues and 33 adjacent tissues were obtained from CC patients admitted to our hospital between March 2012 and June 2014. Real-time polymerase chain reaction and western blotting were performed to analyze the expression of RASAL2 mRNA and protein in these tissues, CC cell lines, and normal cervical cells. Over-expression and silencing of RASAL2 were induced after transfection, and the migration, invasion, and proliferation of the CC cell lines were examined. Results: RASAL2 mRNA and protein expressions were significantly down-regulated in CC tissues and cell lines than in adjacent tissues and normal cervical cells, respectively. While low RASAL2 expression correlated with advanced stage and metastasis of CC, its over-expression significantly inhibited proliferation and metastasis of CC cells and induced apoptosis. Under in vitro conditions, silencing of RASAL2 expression could significantly increase the proliferation, invasion, and migration of CC cells. Conclusion: RASAL2 functioned as a tumor suppressor in CC, and was down-regulated in CC tissue samples and cell lines.

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