Recombinant expression of different mutant K-ras gene in pancreatic cancer Bxpc-3 cells and its effects on chemotherapy sensitivityReport as inadecuate




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Science China Life Sciences

, Volume 57, Issue 10, pp 1011–1017

First Online: 12 September 2014Received: 28 June 2014Accepted: 24 July 2014DOI: 10.1007-s11427-014-4724-0

Cite this article as: Shao, T., Zheng, Y., Zhao, B. et al. Sci. China Life Sci. 2014 57: 1011. doi:10.1007-s11427-014-4724-0

Abstract

K-ras is a member of ras gene family which is involved in cell survival, proliferation and differentiation. When a mutation occurs in ras gene, the activation of Ras proteins may be prolonged to induce oncogenesis. However, the relationship between K-ras mutation and clinical outcomes in pancreatic cancer patients treated with chemotherapy agents is still under debate. In this study, we constructed five pAcGFP1-C3 plasmids for different types of K-ras gene WT, G12V, G12R, G12D, and G13D and stably transfected human pancreatic cancer Bxpc-3 cells with these genes. The wild type and mutant clones showed a comparable growth and expression of K-Ras-GFP fusion protein. The expression of some K-ras mutations resulted in a reduced sensitivity to gefitinib, 5-FU, docetaxel and gemcitabine, while showed no effects on erlotinib or cisplatin. Moreover, compared with the wild type clone, K-Ras downstream signals phospho-Akt and-or phospho-Erk were increased in K-ras mutant clones. Interestingly, different types of K-ras mutation had non-identical K-Ras downstream signal activities and drug responses. Our results are the first to reveal the relationship between different K-ras mutation and drug sensitivities of these anti-cancer drugs in pancreatic cancer cells in vitro.

Keywordscancer chemotherapeutic anti-cancer drug K-ras mutation plasmids pancreas This article is published with open access at link.springer.com

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Author: TengFei Shao - YuanTing Zheng - Bei Zhao - Tao Li - KeGuang Cheng - WeiMin Cai

Source: https://link.springer.com/



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