Inhibition of human 67-kDa laminin receptor sensitizes multidrug resistance colon cancer cell line SW480 for apoptosis induction
| Autor: | Tao Wu, Jian Xu, Chun-Lei Lu, Hao-Jie Yao, Jie-Ming Li, Guozhong Wu, Kun-lun Luo |
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| Rok vydání: | 2015 |
| Předmět: |
Ribosomal Proteins
0301 basic medicine Cell Antineoplastic Agents Apoptosis Receptors Laminin Inhibitory Concentration 50 03 medical and health sciences Laminin Cell Line Tumor Cell Adhesion medicine Humans RNA Small Interfering Cell adhesion Gene knockdown biology General Medicine Drug Resistance Multiple digestive system diseases Extracellular Matrix Gene Expression Regulation Neoplastic Multiple drug resistance 67 kDa Laminin Receptor 030104 developmental biology medicine.anatomical_structure Proto-Oncogene Proteins c-bcl-2 Drug Resistance Neoplasm Colonic Neoplasms Immunology Cancer cell biology.protein Cancer research RNA Interference Fluorouracil Cisplatin |
| Zdroj: | Tumor Biology. 37:1319-1325 |
| ISSN: | 1423-0380 1010-4283 |
| Popis: | The adhesion mediated drug resistance in cancer cells resulted from adhesion of the extracellular matrix is a major cause for multidrug resistance (MDR) and leads chemotherapeutic failure for colon cancer. In this study, we explored the role of 67-kDa laminin receptor (67LR) in chemotherapeutic drug resistance in colon cancer cells. SiRNA-mediated knockdown of 67LR decreased the cell adhesion when laminins were applied. Moreover, 67LR knockdown increased the expression of pro-apoptotic gene Bax but inhibited the expression of anti-apoptotic gene Bcl-2. Enhanced apoptosis was observed in 67LR siRNA-transfected SW480 cell when the cell was treated with doxorubicin for apoptosis induction. Furthermore, MTT assay revealed that the IC50 of chemotherapeutic toward SW480 cell adhesion to laminins was reduced after 67LR knockdown, indicating there was a significant increase of drug sensitivity in SW480 cell. In conclusion, our study demonstrated that 67LR plays a considerable role in the development of colon cancer MDR. |
| Databáze: | OpenAIRE |
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