Abstract
Long non-coding RNAs (IncRNAs), which have evolved as important gene expression modulators, are involved in human malignancies. The down-regulation of IncRNA growth arrest specific transcript 5 (GAS5) has been reported in several cancers, however, the underlying mechanism of IncRNA GAS5 in stomach cancer is poorly understood. In this study, we found that IncRNA GAS5 had lower expression in stomach cancer tissues than the normal counterparts. IncRNA GAS5 was shown to interact with Y-box binding protein 1 (YBX1), and IncRNA GAS5 knockdown was shown to accelerate YBX1 protein turnover without affecting YBX1 transcription. IncRNA GAS5 down-regulation reduced the YBX1 protein level, which decreased YBX1-transactivated p21 expression and abolished G1 phase cell cycle arrest in stomach cancer. These results delineate a novel mechanism of IncRNA GAS5 in suppressing stomach carcinogenesis, and the IncRNA GAS5/YBX1/p21 pathway we discovered may provide useful targets for developing IncRNA-based therapies for stomach cancer.
Original language | English (US) |
---|---|
Article number | 10159 |
Journal | Scientific Reports |
Volume | 5 |
DOIs | |
State | Published - May 11 2015 |
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IncRNA GAS5 enhances G1 cell cycle arrest via binding to YBX1 to regulate p21 expression in stomach cancer. / Liu, Yongchao; Zhao, Jing; Zhang, Wenhong; Gan, Jun; Hu, Chengen; Huang, Guangjian; Zhang, Ying.
In: Scientific Reports, Vol. 5, 10159, 11.05.2015.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - IncRNA GAS5 enhances G1 cell cycle arrest via binding to YBX1 to regulate p21 expression in stomach cancer
AU - Liu, Yongchao
AU - Zhao, Jing
AU - Zhang, Wenhong
AU - Gan, Jun
AU - Hu, Chengen
AU - Huang, Guangjian
AU - Zhang, Ying
PY - 2015/5/11
Y1 - 2015/5/11
N2 - Long non-coding RNAs (IncRNAs), which have evolved as important gene expression modulators, are involved in human malignancies. The down-regulation of IncRNA growth arrest specific transcript 5 (GAS5) has been reported in several cancers, however, the underlying mechanism of IncRNA GAS5 in stomach cancer is poorly understood. In this study, we found that IncRNA GAS5 had lower expression in stomach cancer tissues than the normal counterparts. IncRNA GAS5 was shown to interact with Y-box binding protein 1 (YBX1), and IncRNA GAS5 knockdown was shown to accelerate YBX1 protein turnover without affecting YBX1 transcription. IncRNA GAS5 down-regulation reduced the YBX1 protein level, which decreased YBX1-transactivated p21 expression and abolished G1 phase cell cycle arrest in stomach cancer. These results delineate a novel mechanism of IncRNA GAS5 in suppressing stomach carcinogenesis, and the IncRNA GAS5/YBX1/p21 pathway we discovered may provide useful targets for developing IncRNA-based therapies for stomach cancer.
AB - Long non-coding RNAs (IncRNAs), which have evolved as important gene expression modulators, are involved in human malignancies. The down-regulation of IncRNA growth arrest specific transcript 5 (GAS5) has been reported in several cancers, however, the underlying mechanism of IncRNA GAS5 in stomach cancer is poorly understood. In this study, we found that IncRNA GAS5 had lower expression in stomach cancer tissues than the normal counterparts. IncRNA GAS5 was shown to interact with Y-box binding protein 1 (YBX1), and IncRNA GAS5 knockdown was shown to accelerate YBX1 protein turnover without affecting YBX1 transcription. IncRNA GAS5 down-regulation reduced the YBX1 protein level, which decreased YBX1-transactivated p21 expression and abolished G1 phase cell cycle arrest in stomach cancer. These results delineate a novel mechanism of IncRNA GAS5 in suppressing stomach carcinogenesis, and the IncRNA GAS5/YBX1/p21 pathway we discovered may provide useful targets for developing IncRNA-based therapies for stomach cancer.
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UR - http://www.scopus.com/inward/citedby.url?scp=84929159456&partnerID=8YFLogxK
U2 - 10.1038/srep10159
DO - 10.1038/srep10159
M3 - Article
C2 - 25959498
AN - SCOPUS:84929159456
VL - 5
JO - Scientific Reports
JF - Scientific Reports
SN - 2045-2322
M1 - 10159
ER -