Histone deacetylase 5 promotes Wilms' tumor cell proliferation through the upregulation of c-Met

• Published in: Molecular medicine reports Vol. 13; no. 3; pp. 2745 - 2750
• Main Authors: CAO, XU, LIU, DE-HONG, ZHOU, YUN, YAN, XIANG-MING, YUAN, LI-QUN, PAN, JIAN, FU, MING-CUI, ZHANG, TING, WANG, JIAN
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01.03.2016; Spandidos Publications; Spandidos Publications UK Ltd
• Subjects: Apoptosis; Biotechnology; Bromodeoxyuridine; c-Met; c-Met protein; Cell cycle; Cell growth; Cell Line, Tumor; Cell Proliferation; Child, Preschool; Development and progression; Enzymes; Female; Gene Expression; Gene regulation; Genetic aspects; Health aspects; Histone deacetylase; histone deacetylase 5; Histone Deacetylases - genetics; Histone Deacetylases - metabolism; Humans; Hydrolases; Immunoglobulins; Infant; Kidney Neoplasms - enzymology; Kidney Neoplasms - pathology; Kinases; Liver cancer; Male; Metastasis; Nephroblastoma; Pathogenesis; Properties; Receptor Protein-Tyrosine Kinases - genetics; Receptor Protein-Tyrosine Kinases - metabolism; Rodents; siRNA; Studies; Surgery; Transcription; Tumor cells; Up-Regulation; Wilms Tumor - enzymology; Wilms Tumor - pathology; Wilms' tumor; United States > US; China
• ISSN: 1791-2997; 1791-3004; 1791-3004
• DOI: 10.3892/mmr.2016.4828

The histone deacetylase (HDAC) family is comprised of enzymes, which are involved in modulating the majority of critical cellular processes, including transcriptional regulation, apoptosis, proliferation and cell cycle progression. However, the biological function of HDAC5 in Wilms' tumor remains to be fully elucidated. The present study aimed to investigate the expression and function of HDAC5 in Wilm's tumor. It was demonstrated that the mRNA and protein levels of HDAC5 were upregulated in human Wilms' tumor tissues. Overexpression of HDAC5 in G401 cells was observed to significantly promote cellular proliferation, as demonstrated by the results of an MTT assay and bromodeoxyuridine incorporation assay. By contrast, HDAC5 knockdown using small interfering RNA suppressed the proliferation of the G401 cells. At the molecular level, the present study demonstrated that HDAC5 promoted the expression of c-Met, which has been previously identified as an oncogene. In addition, downregulation of c-Met inhibited the proliferative effects of HDAC5 in human Wilms' tumor cells. Taken together, these results suggested that HDAC5 promotes cellular proliferation through the upregulation of c-Met, and may provide a novel therapeutic target for the treatment of patients with Wilms' tumor.