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Int. J. Mol. Sci. 2013, 14(12), 24399-24411; doi:10.3390/ijms141224399

Cbl-b Enhances Sensitivity to 5-Fluorouracil via EGFR- and Mitochondria-Mediated Pathways in Gastric Cancer Cells

Department of Medical Oncology, the First Hospital of China Medical University, Shenyang 110001, China
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Received: 17 September 2013 / Revised: 26 November 2013 / Accepted: 9 December 2013 / Published: 16 December 2013
(This article belongs to the Section Biochemistry, Molecular Biology and Biophysics)
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Abstract

5-Fluorouracil (5-FU) is an essential component of anticancer chemotherapy against gastric cancer. However, the response rate of single drug is still limited. The ubiquitin ligase Cbl-b is a negative regulator of growth factor receptor signaling and is involved in the suppression of cancer cell proliferation. However, whether Cbl-b could affect 5-FU sensitivity remains unclear. The present study showed that Cbl-b knockdown caused higher proliferation concomitant with the decrease of apoptosis induced by 5-FU treatment in gastric cancer cell. Further mechanism investigation demonstrated that Cbl-b knockdown caused significant increase of phosphorylation of EGFR, ERK and Akt, decrease of mitochondrial membrane potential, and increase of expression ratio of Bcl-2/Bax. These results suggest that Cbl-b enhances sensitivity to 5-FU via EGFR- and mitochondria-mediated pathways in gastric cancer cells.
Keywords: Cbl-b; 5-fluorouracil; EGFR; ERK; PI3k/Akt; gastric cancer Cbl-b; 5-fluorouracil; EGFR; ERK; PI3k/Akt; gastric cancer
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Feng, D.; Ma, Y.; Liu, J.; Xu, L.; Zhang, Y.; Qu, J.; Liu, Y.; Qu, X. Cbl-b Enhances Sensitivity to 5-Fluorouracil via EGFR- and Mitochondria-Mediated Pathways in Gastric Cancer Cells. Int. J. Mol. Sci. 2013, 14, 24399-24411.

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