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Your search keyword '"Xiang-Ming Yan"' showing total 2 results
Start Over Author "Xiang-Ming Yan" Topic gene expression
2 results on '"Xiang-Ming Yan"'

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

Author

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

2. Nuclear paraspeckle assembly transcript 1 promotes the metastasis and epithelial-mesenchymal transition of hepatoblastoma cells by inhibiting miR-129-5p.

Author

MING-CUI FU, LI-QUN YUAN, TING ZHANG, XIANG-MING YAN, YUN ZHOU, HONG-LIANG XIA, YI WU, LI-XIAO XU, XU CAO, and JIAN WANG

Subjects
METASTASIS, LIVER cancer, MICRORNA, GENE expression, CANCER invasiveness
Abstract

The abnormal expression of nuclear paraspeckle assembly transcript 1 (NEAT1) may serve critical functions for the development and progression of various types of human tumor. However, the expression and biological function of NEAT1 in hepatoblastoma (HB) and the underlying mechanisms for the function of NEAT1 in HB remain largely uncharacterized. In the present study, the results of reverse transcription-quantitative polymerase chain reaction revealed that the expression of NEAT1 was significantly elevated in HB tissues. HB tissues with metastasis also exhibited significantly increased levels of NEAT1 compared with tissues without metastasis. The biological functions of NEAT1 were then assessed using gain-/loss-of-function studies. The results of in vitro assays revealed that inhibiting NEAT1 expression reduced the migration and invasion of HepG2 cells. By contrast, the induced expression of NEAT1 exhibited the opposite effect. The present study also demonstrated that the inhibition of NEAT1 expression prevented the epithelial-mesenchymal transition of HepG2 cells, whereas forced expression of NEAT1 exhibited the opposite effect. In addition, it was confirmed that NEAT1 could modulate the expression of microRNA (miR)-129-5p in HepG2 cells, and that NEAT1 may exert its effect on the metastatic behaviors and epithelial-mesenchymal transition of HepG2 cells by inhibiting miR-129-5p. In conclusion, the present study indicated that NEAT1 expression was aberrantly increased in HB and that it may promote the metastasis of HB cells by inhibiting miR-129-5p. Targeting NEAT1 may potentially be a novel therapeutic option for treating patients with HB. [ABSTRACT FROM AUTHOR]

Published
2017
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