4.2 Article

MicroRNA-29a Promotes Pancreatic Cancer Growth by Inhibiting Tristetraprolin

期刊

CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 37, 期 2, 页码 707-718

出版社

Cell Physiol Biochem Press GmbH & Co
DOI: 10.1159/000430389

关键词

MicroRNA-29a; Tristetraprolin; Pancreatic cancer

资金

  1. Research Grant of Xinglin Nova Project of Shanghai Municipal Commission of Health and Family Planning [ZY3-RCPY-2-2083]
  2. Key Medical Disciplines of Shanghai Municipal [ZK2012A04]
  3. Research Grant of Shanghai Municipal Commission of Health and Family Planning [20124178]
  4. Research Grant for Traditional Chinese Medicine of Shanghai Municipal Commission of Health and Family Planning [2014LP022A]
  5. Key Project of Shanghai Municipal Commission of Health and Family Planning Supporting Programs [20134036]
  6. Research Grant of Changning District Commission of Health and Family Planning of Shanghai [20144Y015]

向作者/读者索取更多资源

Background/Aims: The microRNA (miR) 29 family has been studied extensively for its involvement in several diseases, and aberrant expression of its members is associated with tumorigenesis and cancer progression. Here, we examined the role of miR-29a in pancreatic cancer and the involvement of tristetraprolin (TTP). Methods: We monitored miR-29a and TTP expression in pancreatic cancer by qRT-PCR and western blotting. The effect of miR-29a on pancreatic cancer was determined through MTT assay and migration assay. The results were validated in the tumorigenesis model. Results: We found that miR-29a was up regulated in pancreatic tumor tissues and cell lines and positively correlated with metastasis. Ectopic expression of miR-29a increased the expression of pro-inflammatory factors and epithelial-mesenchymal transition (EMT) markers, through down regulating TTP. TTP was down regulated in tumor tissues, and its ectopic expression decreased cell viability and migration in vitro, inhibited tumor growth and the EMT phenotype in vivo, and reversed the effect of miR-29a on tumor cell proliferation and invasion in vitro and in vivo. Conclusion: Our results suggest that miR-29a acts as an oncogene by down regulating TTP and provide the basis for further studies exploring the potential of miR-29a and TTP as biomarkers and targets for the treatment of pancreatic cancer. (C) 2015 The Author(s) Published by S. Karger AG, Basel

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