Potential role of TET2 in gastric cancer cisplatin resistance
Autor: | Yuhong Xu, Jun Zhang, Yuzhen Zhou, Dong-Hua Wang, Kun Zhou, Yanli Li, Huan Guo, Dongmei Zhao, Zunrong Zheng |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Antineoplastic Agents Drug resistance Pathology and Forensic Medicine Dioxygenases 03 medical and health sciences 0302 clinical medicine Stomach Neoplasms Cell Line Tumor Proto-Oncogene Proteins Tumor Microenvironment Medicine Humans Interleukin 6 Cisplatin Tumor microenvironment biology business.industry Interleukin-6 Cancer Cell Biology medicine.disease DNA-Binding Proteins Gene Expression Regulation Neoplastic 030104 developmental biology Histone Acetylation Drug Resistance Neoplasm 030220 oncology & carcinogenesis Cancer research biology.protein Demethylase business medicine.drug |
Zdroj: | Pathology, research and practice. 215(11) |
ISSN: | 1618-0631 |
Popis: | Gastric cancer (GC) represents one of the most predominant malignancies with high incidence and mortality rates. Although traditional chemotherapeutics, including cisplatin are effective in the treatment of GC, patients often develop drug resistance in clinic. The present study aimed to explore the underlying mechanism of cisplatin-induced drug resistance in GC. The potential role of DNA demethylase ten-eleven translocation-2 (TET2) in modulating cisplatin resistance of GC cells was investigated. It was observed that TET2 was significantly decreased in cisplatin resistance SGC7901/DDP cells compared with non-resistant cells and TET2 overexpression markedly reduced the tolerance to cisplatin. Additionally, evidence was provided that TET2 regulated interleukin-6 levels in the tumor microenvironment through histone acetylation and therefore served an important role in the development of cisplatin resistance in GC cells. Taken together, the results suggested that TET2-mediated cisplatin resistance may represent a novel mechanism of drug resistance in GC cells and may offer novel treatment approaches. |
Databáze: | OpenAIRE |
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