ERp29 downregulation enhances lung adenocarcinoma cell chemosensitivity to gemcitabine by upregulating HSP27 phosphorylation
Autor: | Zhijun Li, Tingyu Tang, Guangyue Qin, Xiaoxi Zhou, Wu Ye, Jianzong Du, Xuefang Li, Haiyan Wu |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Cancer Research biology Oncogene Chemistry Cell Articles General Medicine Cell cycle medicine.disease Gemcitabine 03 medical and health sciences 030104 developmental biology 0302 clinical medicine medicine.anatomical_structure Immunology and Microbiology (miscellaneous) Downregulation and upregulation Hsp27 Apoptosis 030220 oncology & carcinogenesis medicine Cancer research biology.protein Adenocarcinoma medicine.drug |
Zdroj: | Experimental and therapeutic medicine. 17(1) |
ISSN: | 1792-0981 |
Popis: | The aim of the current study was to assess the underlying mechanism of endoplasmic reticulum protein 29 (ERp29) in lung adenocarcinoma chemosensitivity to gemcitabine. Western blot analysis was performed to detect ERp29 expression following lung adenocarcinoma cell treatment with gemcitabine. The effects of gemcitabine in combination with ERp29 siRNA on cell apoptosis, cell cycle and heat shock protein 27 (HSP27) expression were assessed. The results demonstrated that ERp29 expression was increased on exposure to gemcitabine. The apoptotic rate of lung adenocarcinoma cells were also increased following gemcitabine treatment and the combined application of gemcitabine and ERp29 siRNA synergistically increased apoptotic rates further. It was also revealed that gemcitabine and ERp29 siRNA synergistically increased the ratio of phosphorylated to total HSP27 protein. In addition, downregulation of HSP27 significantly reduced lung adenocarcinoma chemosensitivity to gemcitabine. These data indicate that ERp29 affects lung adenocarcinoma cell chemosensitivity to gemcitabine by regulating phosphorylated HSP27. ERp29 is a novel target, which may be used to enhance the therapeutic effect of lung adenocarcinoma treatment with gemcitabine. |
Databáze: | OpenAIRE |
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