Title of article :
Chmp1A acts as a tumor suppressor gene that inhibits proliferation of renal cell carcinoma
Author/Authors :
You، نويسنده , , Zhenqiang and Xin، نويسنده , , Yanfei and Liu، نويسنده , , Yan and Sun، نويسنده , , Junying and Zhou، نويسنده , , Guoliang and Gao، نويسنده , , Haiyan and Xu، نويسنده , , Pansheng and Chen، نويسنده , , Yunxiang and Chen، نويسنده , , Guochan and Zhang، نويسنده , , Lijiang and Gu، نويسنده , , Liqiang and Chen، نويسنده , , Zhiqin and Han، نويسنده , , Ni-Bin and Xuan، نويسنده , , Yaoxian، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2012
Pages :
7
From page :
190
To page :
196
Abstract :
Renal cell carcinoma (RCC) is a highly malignant and often fatal disease of the kidney. Chmp1A is a member of the Endosomal Sorting Complex Required for Transport (ESCRT-III) family, and plays a role in the cytoplasm in sorting proteins to the multivesicular body (MVB). Chmp1A functions as a tumor suppressor gene and has been reported in pancreatic tumor cells. Here, we examined the expression level of Chmp1A in human RCC tissues and renal tumor cells by real-time quantitative RT-PCR and western blot. We found that the expression level of Chmp1A is significantly lower in RCC tissues and renal tumor cells compared with adjacent non-tumorous tissues and normal renal cells. Additionally, inhibition of Chmp1A expression by shRNA induced tumor formation in normal renal cells. However, inhibition of Chmp1A did not significantly affect tumor cell proliferation in vitro and tumor progression in vivo. Interestingly, overexpression of Chmp1A using a eukaryotic plasmid inhibited the proliferation of renal tumor cells in vitro and the growth of renal tumor in vivo. Thus, our results demonstrate that Chmp1A functions as a tumor suppressor gene in renal cells and may be a useful target for treatment of RCC.
Keywords :
Tumor suppressor , Chromatin modifying protein 1A (Chmp1A) , Renal cell carcinoma (RCC)
Journal title :
Cancer Letters
Serial Year :
2012
Journal title :
Cancer Letters
Record number :
1821356
Link To Document :
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