DNA methylation downregulated mir-10b acts as a tumor suppressor in gastric cancer
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- 作者：Zheng Li (1) (2)
Huizi Lei (2) (3)
Min Luo (2)
Yi Wang (4)
Lei Dong (2)
Yanni Ma (2)
Changzheng Liu (2)
Wei Song (2)
Fang Wang (2)
Junwu Zhang (2)
Jianxiong Shen (1)
Jia Yu (2) - 关键词：Gastric cancer ; miR ; 10b ; Tumor suppressor ; Methylation
- 刊名：Gastric Cancer
- 出版年：2015
- 出版时间：January 2015
- 年：2015
- 卷：18
- 期：1
- 页码：43-54
- 全文大小：4,964 KB
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17. Kim K, Lee HC, Park JL, Kim M, Kim SY, Noh SM, et al. Epigenetic regulation of micro - 作者单位：Zheng Li (1) (2)
Huizi Lei (2) (3)
Min Luo (2)
Yi Wang (4)
Lei Dong (2)
Yanni Ma (2)
Changzheng Liu (2)
Wei Song (2)
Fang Wang (2)
Junwu Zhang (2)
Jianxiong Shen (1)
Jia Yu (2)
1. Department of Orthopedic Surgery, Peking Union Medical College Hospital, Peking Union Medical College, Beijing, 100005, People’s Republic of China
2. Department of Biochemistry, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences (CAMS), Peking Union Medical College (PUMC), Beijing, 100005, People’s Republic of China
3. Department of Pathology, Cancer Institute and Hospital, Chinese Academy of Medical Sciences, Beijing, 100021, People’s Republic of China
4. Department of VIP, Cancer Institute and Hospital, Chinese Academy of Medical Sciences, Beijing, 100021, People’s Republic of China - ISSN：1436-3305
文摘
Background MicroRNAs act as tumor suppressors or oncogenes. The pathological roles of miRNAs in gastric tumorigenesis are largely unknown. Although miR-10b was identified as an miRNA deregulator expressed in gastric cancer (GC), there also exists some debate on whether miR-10b is acting as tumor suppressor or oncogene in GC. Methods Quantitative RT-PCR was employed to investigate the level of miR-10b in GC tissues and matched adjacent normal tissues (n?=?100). In vitro cell proliferation, apoptosis assays, cell migration, and invasion assays were performed to elucidate the biological effects of miR-10b. Because silencing of miRNA by promoter CpG island methylation may be an important mechanism in tumorigenesis, GC cells were treated with 5-aza-2-deoxycytidine and trichostatin A, and expression changes of miR-10b were subsequently examined by quantitative RT-PCR. Furthermore, the methylation status of the CpG island upstream of miR-10b was analyzed by methylation-specific PCR in GC tissues (n?=?29). Results We showed here that miR-10b was significantly downregulated in GC cell lines and tissues as demonstrated by quantitative real-time PCR. Overexpression of miR-10b in MGC-803 and HGC-27 dramatically suppressed cell proliferation, migration, invasion, and induced apoptosis. Moreover, we demonstrated that T-cell lymphoma invasion and metastasis (Tiam1) was a target of miR-10b. Furthermore, 5-aza-2-deoxycytidine and trichostain A increased miR-10b expression, and the methylation level was high in the CpG islands upstream of miR-10b gene. Conclusions Taken together, these findings suggest that miR-10b may function as a novel tumor suppressor and is partially silenced by DNA hypermethylation in GC.