1. Rejection of adenovirus infection is independent of coxsackie and adenovirus receptor expression in cisplatin-resistant human lung cancer cells
- Author
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Ya Ding, Xiao Shi Zhang, Rui Qing Peng, and Nian Hua Zhang
- Subjects
0301 basic medicine ,Coxsackie and Adenovirus Receptor-Like Membrane Protein ,Cancer Research ,Lung Neoplasms ,Leupeptins ,medicine.drug_class ,Adenoviridae Infections ,Receptor expression ,Adenocarcinoma of Lung ,Adenocarcinoma ,Biology ,Hydroxamic Acids ,medicine.disease_cause ,Adenoviridae ,03 medical and health sciences ,0302 clinical medicine ,Cell Line, Tumor ,medicine ,Humans ,Adenovirus infection ,Oncogene ,Histone deacetylase inhibitor ,General Medicine ,respiratory system ,medicine.disease ,respiratory tract diseases ,Histone Deacetylase Inhibitors ,030104 developmental biology ,Trichostatin A ,Oncology ,A549 Cells ,Drug Resistance, Neoplasm ,Cell culture ,030220 oncology & carcinogenesis ,Cancer research ,Proteasome inhibitor ,Cisplatin ,Proteasome Inhibitors ,medicine.drug - Abstract
The adenovirus vector-based cancer gene therapy is controversial. Low transduction efficacy is believed to be one of the main barriers for the decreased expression of coxsackie and adenovirus receptor (CAR) on tumor cells. However, the expression of CAR on primary tumor tissue and tumor tissue survived from treatment has still been not extensively studied. The present study analyzed the adenovirus infection rates and CAR expression in human lung adenocarcinoma cell line A549 and its cisplatin-resistant subline A549/DDP. The results showed that although the CAR expression in A549 and A549/DDP was not different, compared with the A549, A549/DDP appeared obviously to reject adenovirus infection. Moreover, we modified CAR expression in the two cell lines with proteasome inhibitor MG-132 and histone deacetylase inhibitor trichostatin A (TSA), and analyzed the adenovirus infection rates after modifying agent treatments. Both TSA and MG-132 pretreatments could increase the CAR expression in the two cell lines, but the drug pretreatments could only make A549 cells more susceptible to adenovirus infectivity.
- Published
- 2016