Overexpression of AGR2 Is Associated With Drug Resistance in Mutant Non-small Cell Lung Cancers
Autor: | Thi-Thu-Trang Luu, Sang Kook Lee, Ruoci Hu, Duc-Hiep Bach, Donghwa Kim, Hyen Joo Park |
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Rok vydání: | 2020 |
Předmět: |
Cancer Research
Cell Survival AGR2 Apoptosis Drug resistance Biology Immunofluorescence 03 medical and health sciences Erlotinib Hydrochloride 0302 clinical medicine Gefitinib Mucoproteins Cell Movement Carcinoma Non-Small-Cell Lung medicine Humans Neoplasm Invasiveness Viability assay neoplasms Protein Kinase Inhibitors Cell Proliferation Oncogene Proteins medicine.diagnostic_test General Medicine respiratory tract diseases ErbB Receptors Gene Expression Regulation Neoplastic Oncology Drug Resistance Neoplasm 030220 oncology & carcinogenesis Cancer cell Mutation Cancer research Quinazolines Immunohistochemistry Erlotinib medicine.drug |
Zdroj: | Anticancer research. 40(4) |
ISSN: | 1791-7530 |
Popis: | Background/aim The resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), such as gefitinib or erlotinib, is considered a major challenge in the treatment of patients with non-small cell lung cancer (NSCLC). Herein, we identified the critical roles of anterior gradient 2 (AGR2) in gefitinib (Gef) resistance of mutant NSCLC cells. Materials and methods Using datasets from a pair of NSCLC-sensitive and NSCLC-resistant cells, immunoblotting, immunofluorescence and immunohistochemistry, and cell viability assays were applied to identify the effects of AGR2. Results AGR2 was found to be significantly over-expressed in Gef-resistant cells and was highly associated with drug resistance, proliferation, migration, and invasion of cancer cells. Moreover, AGR2 and ADAMTS6 formed a negative feedback loop in drug-resistant cells. Conclusion Modulation of overexpression of AGR2 in mutant NSCLC cells may be an attractive therapeutic strategy for the treatment of EGFR-TKI-resistant NSCLC. |
Databáze: | OpenAIRE |
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