1. Histone deacetylase 5 promotes Wilms' tumor cell proliferation through the upregulation of c-Met
- Author
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Jian Pan, Li‑Qun Yuan, Yun Zhou, Xiang‑Ming Yan, Xu Cao, De‑Hong Liu, Ming‑Cui Fu, Ting Zhang, and Jian Wang
- Subjects
0301 basic medicine ,Male ,Cancer Research ,C-Met ,Gene Expression ,Biology ,Biochemistry ,Wilms Tumor ,Histone Deacetylases ,03 medical and health sciences ,chemistry.chemical_compound ,Downregulation and upregulation ,Cell Line, Tumor ,Genetics ,Transcriptional regulation ,medicine ,Humans ,Molecular Biology ,Cell Proliferation ,Histone deacetylase 5 ,Oncogene ,Infant ,Receptor Protein-Tyrosine Kinases ,Wilms' tumor ,Cell cycle ,medicine.disease ,Kidney Neoplasms ,Up-Regulation ,030104 developmental biology ,Oncology ,chemistry ,Child, Preschool ,Cancer research ,Molecular Medicine ,Female ,Histone deacetylase - Abstract
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.
- Published
- 2014