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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Wu, Zhonghua Wang, Zhongqi Xu, Zhenye Zhao, Xiaozhen Gong, Yabin Zhou, Lijuan Xiang, Yi |
| Description | Author Affiliation: Zhao X ( Department of Oncology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.); Xu Z ( Department of Oncology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.); Wang Z ( Department of Oncology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.); Wu Z ( Experiment Center for Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China.); Gong Y ( Department of Oncology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.); Zhou L ( Department of Oncology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.); Xiang Y ( Department of Oncology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.) |
| Abstract | The expression of integrin-linked kinase (ILK) has been reported to be involved in the regulation of integrin-mediated processes, including cancer cell proliferation, migration and invasion. Previous studies have demonstrated that inhibition of ILK may be an underlying approach for treating cancer. However, whether the knock down of ILK affects growth and apoptosis of lung cancer cells remains to be elucidated. Importantly, whether downregulation of ILK increases the sensitivity of lung cancer cells to cisplatin and amplifies cell apoptosis also remains to be elucidated. In the present study, ILK downregulation was mediated by lentivirus-mediated RNA interference. The expression levels of associated genes were determined by reverse-transcription quantitative polymerase chain reaction and western blotting. Cell proliferation was evaluated using a modified 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and clone formation assay. The cell cycle and apoptosis were analyzed using flow cytometry. The current data revealed that lentivirus-mediated ILK gene silencing alone inhibited A549 cell proliferation and promotes cell cycle arrest, however, had no detectable effect on cell apoptosis. However, combined treatment with lentivirus-mediated ILK interference and cisplatin chemotherapy induced significantly more cell apoptosis than mono-chemotherapy or knockdown. The increased cell apoptosis and proliferation inhibition were attributed to abnormal downstream protein expression of ILK, including phospho-glycogen synthase kinase 3ß, p-AKT, activator protein-1, ß-catenin, cyclin D1 and matrix metalloproteinase-9. ILK inhibition may suppress the proliferation of A549 and increase A549 sensitivity to cisplatin. The combined treatment of ILK gene knockdown and chemotherapy has the potential to improve anticancer efficacy. |
| ISSN | 17912997 |
| e-ISSN | 17913004 |
| DOI | 10.3892/mmr.2015.3471 |
| Journal | Molecular Medicine Reports |
| Issue Number | 1 |
| Volume Number | 12 |
| Language | English |
| Publisher | Spandidos Publications |
| Publisher Date | 2015-07-01 |
| Publisher Place | Greece |
| Access Restriction | Open |
| Subject Keyword | Antineoplastic Agents Pharmacology Cisplatin Drug Resistance, Neoplasm Drug Effects Epithelial Cells Gene Expression Regulation, Neoplastic Lentivirus Genetics Rna Interference Apoptosis Cell Cycle Checkpoints Cell Line, Tumor Cell Proliferation Cyclin D1 Metabolism Pathology Genetic Vectors Glycogen Synthase Kinase 3 Matrix Metalloproteinase 9 Protein-serine-threonine Kinases Proto-oncogene Proteins C-akt Respiratory Mucosa Signal Transduction Transcription Factor Ap-1 Beta Catenin Research Support, Non-u.s. Gov't Discipline Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology |
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