Journal of Gastroenterology

, Volume 44, Issue 6, pp 556–561 | Cite as

Down-regulation of miR-141 in gastric cancer and its involvement in cell growth

  • Ying Du
  • Yanjun Xu
  • Ling Ding
  • Haomi Yao
  • Hong Yu
  • Tianhua ZhouEmail author
  • Jianmin SiEmail author
Original Article—Alimentary Tract



Human microRNA-141 (miR-141), a member of the miR-200 family, has been reported to be associated with various human malignancies. However, it remains unknown whether miR-141 is involved in the pathogenesis of gastric cancer. Therefore, we examined the expression of miR-141 in gastric cancer tissues and the effect of miR-141 overexpression on cancer cell proliferation.


The expression level of miR-141 in 35 pair-matched gastric neoplastic and adjacent non-neoplastic tissues, and in 5 gastric cancer cell lines were examined by quantitative real-time PCR. The growth of MGC-803 cells transfected with miRNA precursor was examined by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazoliumbromide) assay.


MiR-141 was significantly down-regulated in 80% (28/35) of primary gastric cancer tissues compared with pair-matched adjacent non-tumor tissues (P < 0.01). The expression of miR-141 was also found to be substantially reduced in several human gastric cancer cell lines such as MGC-803, HGC-27, SGC-7901 and BGC-823 cells. Overexpression of miR-141 with its precursors significantly inhibited the proliferation of gastric cancer cells.


These results suggest that miR-141 may be involved in the development of gastric cancer through its inhibitory effect on cell proliferation.


MiR-141 Gastric cancer MGC-803 cell Cell proliferation 



We thank Xunyan Liu for her technical help. The study was supported by a grant from the National High Technology Research and Development Program of China (No. 2006AA02Z470), a joint grant from National Ministry of Public Health and Zhejiang Province (WKJ2006-2-012 and -014), a grant from the Medicine Science Foundation of Zhejiang Province (No. 2008A041), a grant from National Ministry of Education (NCET-06-0530) and two grants from Natural Scientific Foundation of Zhejiang Province (R205291 and 2007R10G2010103).

Supplementary material

535_2009_37_MOESM1_ESM.doc (28 kb)
Supplementary Table S1 (DOC 28 kb)
535_2009_37_MOESM2_ESM.eps (8.3 mb)
Supplementary Fig. S1 (EPS 8496 kb)


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Copyright information

© Springer 2009

Authors and Affiliations

  1. 1.Gastroenterology Laboratory, Clinical Research Institute, Sir Run Run Shaw HospitalZhejiang University School of MedicineHangzhouPeople’s Republic of China
  2. 2.The Center for Diseases ModelingZhejiang University School of MedicineHangzhouPeople’s Republic of China

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