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已发表论文
整合素连接激酶在肺癌耐药中的作用
Authors Jia Z
Published Date June 2015 Volume 2015:8 Pages 1561—1565
DOI http://dx.doi.org/10.2147/OTT.S81447
Received 23 January 2015, Accepted 13 April 2015, Published 23 June 2015
Approved for publication by Professor Jianmin Xu
Objective: The objective of the present investigation was to investigate the role of integrin-linked kinase (ILK) in the gemcitabine-resistant lung cancer cell line A549 and explore the underlying mechanism.
Materials and methods: Gemcitabine-resistant A549 (A549/GemR) cell line was established by pulse-exposed to moderate concentration of gemcitabine (Gem), and the drug resistant index was measured by MTT assay. Expression of ILK in A549/GemR cell line was detected by Western blot and real-time PCR. An ILK gene-silencing cell line was constructed using lentivirus-coated ILK shRNA. MTT assay was used to detect the drug sensitivity of the A549/GemR cell line to Gem after the ILK gene silencing. Western blot was used to measure the expression of E-cadherin, fibronectin, and MRP1 (multidrug resistance-associated protein 1) after silencing the ILK gene.
Result: The drug resistance index of A549/GemR was 13.5, and the messenger RNA and protein level of ILK was increased in A549/GemR. IC50 (half maximal inhibitory concentration) decreased from 14.69 to 4.13 mg/L when ILK was knocked down in A549/GemR. The expression of fibronectin and MRP1 was upregulated and E-cadherin expression was downregulated in A549/GemR, and these changes were reversed after ILK was knocked down.
Conclusion: ILK was involved in drug resistance to Gem in lung cancer, and this function may be mediated by epithelial–mesenchymal transition and the MRP1 pathway.
Keywords: lung cancer, drug resistance, gemcitabine, ILK, EMT
Materials and methods: Gemcitabine-resistant A549 (A549/GemR) cell line was established by pulse-exposed to moderate concentration of gemcitabine (Gem), and the drug resistant index was measured by MTT assay. Expression of ILK in A549/GemR cell line was detected by Western blot and real-time PCR. An ILK gene-silencing cell line was constructed using lentivirus-coated ILK shRNA. MTT assay was used to detect the drug sensitivity of the A549/GemR cell line to Gem after the ILK gene silencing. Western blot was used to measure the expression of E-cadherin, fibronectin, and MRP1 (multidrug resistance-associated protein 1) after silencing the ILK gene.
Result: The drug resistance index of A549/GemR was 13.5, and the messenger RNA and protein level of ILK was increased in A549/GemR. IC50 (half maximal inhibitory concentration) decreased from 14.69 to 4.13 mg/L when ILK was knocked down in A549/GemR. The expression of fibronectin and MRP1 was upregulated and E-cadherin expression was downregulated in A549/GemR, and these changes were reversed after ILK was knocked down.
Conclusion: ILK was involved in drug resistance to Gem in lung cancer, and this function may be mediated by epithelial–mesenchymal transition and the MRP1 pathway.
Keywords: lung cancer, drug resistance, gemcitabine, ILK, EMT
