| Molecular Cancer | |
| CHD1L: a novel oncogene | |
| Review | |
| Feng Xu1  Wen Cheng1  Yun Su2  | |
| [1] Department of Urology, Nanjing Jinling Hospital, School of Medicine, Nanjing University, 210002, NanjingJiangsu, P.R. of China;Outpatient department of Eastern Division, First Hospital of Nanjing, Nanjing Medical University, Nanjing, P.R. of China; | |
| 关键词: CHD1L; ALC1; Oncogene; Chr1q21; Amplification; ARHGEF9; SPOCK1; Nur77; | |
| DOI : 10.1186/1476-4598-12-170 | |
| received in 2013-08-22, accepted in 2013-12-19, 发布年份 2013 | |
| 来源: Springer | |
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【 摘 要 】
Comprehensive sequencing efforts have revealed the genomic landscapes of common forms of human cancer and ~ 140 driver genes have been identified, but not all of them have been extensively investigated. CHD1L (chromodomain helicase/ATPase DNA binding protein 1-like gene) or ALC1 (amplified in liver cancer 1) is a newly identified oncogene located at Chr1q21 and it is amplified in many solid tumors. Functional studies of CHD1L in hepatocellular carcinoma and other tumors strongly suggested that its oncogenic role in tumorigenesis is through unleashed cell proliferation, G1/S transition and inhibition of apoptosis. The underlying mechanisms of CHD1L activation may disrupt the cell death program via binding the apoptotic protein Nur77 or through activation of the AKT pathway by up-regulation of CHD1L-mediated target genes (e.g., ARHGEF9, SPOCK1 or TCTP). CHD1L is now considered to be a novel independent biomarker for progression, prognosis and survival in several solid tumors. The accumulated knowledge about its functions will provide a focus to search for targeted treatment in specific subtypes of tumors.
【 授权许可】
CC BY
© Cheng et al.; licensee BioMed Central Ltd. 2013
【 预 览 】
| Files | Size | Format | View |
|---|---|---|---|
| RO202311100533429ZK.pdf | 1355KB |
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