Galanin is a novel epigenetic silenced functional tumor suppressor in renal cell carcinoma

Aim: To assess the expression level and function of Galanin in renal cell carcinoma (RCC). Methods: The expression level of Galanin in a series of RCC cell lines (769P, 786-O, A498, Caki-1, and ACHN) was studied. 786-O cells were exposed to pharmacological demethylation to assess the involvement of...

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Bibliographic Details
Published in:Cancer translational medicine 2015-11, Vol.1 (6), p.183-187
Main Authors: Sun, Shengkun, Xu, Axiang, Yang, Guoqiang, Cheng, Yingduan
Format: Article
Language:English
Subjects:
Cell culture
Cell cycle
Cell growth
Colorectal cancer
Conflicts of interest
Deoxyribonucleic acid
DNA
DNA methylation
Epigenetics
Esophagus
Genes
Kinases
Medical prognosis
Neuropeptides
Polymerase chain reaction
Rodents
Signal transduction
Tumorigenesis
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Summary:Aim: To assess the expression level and function of Galanin in renal cell carcinoma (RCC). Methods: The expression level of Galanin in a series of RCC cell lines (769P, 786-O, A498, Caki-1, and ACHN) was studied. 786-O cells were exposed to pharmacological demethylation to assess the involvement of promoter methylation downregulation of Galanin level. Galanin normal expressed ACHN cell line was knockdown with siRNA and was further used to study its role in cell proliferation and invasion. The downstream targets were screened by real time-polymerase chain reaction. Results: Galanin was downregulated in two (786-O and A498) out of five RCC cell lines. Pharmacological demethylation restored the Galanin expression to normal levels in 786-O cells suggesting of its downregulation through promoter methylation. Knockdown of Galanin resulted in increased proliferation and invasion ability of ACHN cells while increasing the expression of oncogenes MYC, CCND1, and FRA1. Conclusion: The above results suggest that Galanin behaves as a tumor suppressor gene in RCC and may be of clinical importance as a potential biomarker and therapeutic target in renal cancer patients.
ISSN:2395-3977
2395-3012
DOI:10.4103/2395-3977.172861