Onco-miR-24 regulates cell growth and apoptosis by targeting BCL2L11 in gastric cancer
Haiyang Zhang , Jingjing Duan , Yanjun Qu , Ting Deng , Rui Liu , Le Zhang , Ming Bai , Jialu Li , Tao Ning , Shaohua Ge , Xia Wang , Zhenzhen Wang , Qian Fan , Hongli Li , Guoguang Ying , Dingzhi Huang , Yi Ba
Protein Cell ›› 2016, Vol. 7 ›› Issue (2) : 141 -151.
Onco-miR-24 regulates cell growth and apoptosis by targeting BCL2L11 in gastric cancer
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.
gastric cancer / BCL2L11 / miR-24 / tumorigenesis / cell apoptosis / proliferation / migration
| [1] |
|
| [2] |
|
| [3] |
|
| [4] |
|
| [5] |
|
| [6] |
|
| [7] |
|
| [8] |
|
| [9] |
|
| [10] |
|
| [11] |
|
| [12] |
|
| [13] |
|
| [14] |
|
| [15] |
|
| [16] |
|
| [17] |
|
| [18] |
|
| [19] |
|
| [20] |
|
| [21] |
|
| [22] |
|
| [23] |
|
| [24] |
|
| [25] |
|
| [26] |
|
| [27] |
|
| [28] |
|
| [29] |
|
| [30] |
|
| [31] |
|
| [32] |
|
| [33] |
|
| [34] |
|
| [35] |
|
| [36] |
|
| [37] |
|
| [38] |
|
| [39] |
|
| [40] |
|
| [41] |
|
| [42] |
|
| [43] |
|
This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
/
| 〈 |
|
〉 |