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To examine the antiproliferative effect of the combination of docetaxel and sorafenib, applied to the representative non-small cell lung cancer cell line A549 cells either wild type or with acquired resistance to docetaxel (A549/D). The aim of this study is to evaluate the synergistic effect of combination treatment on cell growth inhibition and to elucidate the involved molecular mechanisms. A549 cells with acquired resistance to docetaxel were established by continuous exposure to docetaxel. We examined the effect of different combinatorial treatment on cell proliferation and cell cycle distribution. In addition, the effect of combinatorial treatments on proliferative and apoptotic signalling pathway were studied. Our results showed that the synergistic effect presented when A549 cells were treated with docetaxel followed by sorafenib or when A549/D cells were treated in reverse sequence. Furthermore, we suggested that synergistic effect in A549/D cells was caused by inhibiting P-gp function and altering in the balance of growth and apoptotic signalling pathways. Our data suggested a potential role of sorafenib in chemosensitizing docetaxel-resistant cancer cells. This study also provides molecular evidence for applying different therapeutic strategies for patients with different genetic and proteomic profile. © 2013 Springer Science+Business Media New York. Source


You J.,Taizhou Second Peoples Hospital | He X.,Taizhou Second Peoples Hospital | Ding H.,Taizhou Second Peoples Hospital | Zhang T.,Nanjing Southeast University
Cell Biochemistry and Biophysics | Year: 2014

Breast cancer metastasis suppressor 1 (BRMS1) was originally identified as a metastasis suppressor gene in human breast cancer. Previous studies have reported that loss of BRMS1 expression correlates with tumor progression, and poor prognosis in NSCLC. However, the role of BRMS1 in NSCLC is not fully understood. In this study, we found that expression of BRMS1 in A549 cells did not affect cell growth under normal culture conditions but sensitized cells to apoptosis induced by serum deprivation. Consistently, knockdown of endogenous BRMS1 expression in H1299 cells suppressed cell apoptosis. We identified that BRMS1 regulate apoptosis in NSCLC cells by modulating Stat3 activation. Taken together, our results show that BRMS1 sensitizes NSCLC cells to apoptosis through Stat3 signaling pathway, suggesting a potential role of BRMS1 in regulating NSCLC apoptosis and metastasis. © 2014 Springer Science+Business Media New York. Source

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