- Author:
Haiyang ZHANG
1
;
Jingjing DUAN
1
;
Yanjun QU
1
;
Ting DENG
1
;
Rui LIU
1
;
Le ZHANG
1
;
Ming BAI
1
;
Jialu LI
2
;
Tao NING
1
;
Shaohua GE
1
;
Xia WANG
1
;
Zhenzhen WANG
3
;
Qian FAN
1
;
Hongli LI
1
;
Guoguang YING
1
;
Dingzhi HUANG
4
;
Yi BA
5
Author Information
- Publication Type:Journal Article
- Keywords: BCL2L11; cell apoptosis; gastric cancer; miR-24; migration; proliferation; tumorigenesis
- MeSH: Animals; Apoptosis; genetics; Apoptosis Regulatory Proteins; deficiency; genetics; Base Sequence; Bcl-2-Like Protein 11; Cell Line, Tumor; Cell Movement; genetics; Cell Proliferation; genetics; Down-Regulation; genetics; Gene Silencing; Male; Membrane Proteins; deficiency; genetics; Mice; MicroRNAs; genetics; Proto-Oncogene Proteins; deficiency; genetics; Rats; Stomach Neoplasms; genetics; pathology
- From: Protein & Cell 2016;7(2):141-151
- CountryChina
- Language:English
- Abstract: Gastric cancer is one of the most common malignancies worldwide; however, the molecular mechanism in tumorigenesis still needs exploration. BCL2L11 belongs to the BCL-2 family, and acts as a central regulator of the intrinsic apoptotic cascade and mediates cell apoptosis. Although miRNAs have been reported to be involved in each stage of cancer development, the role of miR-24 in GC has not been reported yet. In the present study, miR-24 was found to be up-regulated while the expression of BCL2L11 was inhibited in tumor tissues of GC. Studies from both in vitro and in vivo shown that miR-24 regulates BCL2L11 expression by directly binding with 3'UTR of mRNA, thus promoting cell growth, migration while inhibiting cell apoptosis. Therefore, miR-24 is a novel onco-miRNA that can be potential drug targets for future clinical use.