
Insulin regulates metabolism through homologous receptor tyrosine kinases, and plays a role in proliferation of breast cancer cells. Our research studied whether insulin, administered separately or in combination with paclitaxel, interferes with paclitaxel-mediated biological activity in human breast cancer cells. Not only did insulin influence paclitaxel-mediated cell microtubule reorganization, but it also influenced MCF-7 cell sensitivity to paclitaxel. Furthermore, combined administrations of insulin and paclitaxel affected MAPK pathway, Raf-1 activation and p53 expression levels. Our findings indicate that insulin seems to modulate MCF-7 cell response to paclitaxel; consequently, elevated levels of insulin could influence tumor cell resistance.
Flavonoids, Paclitaxel, Cell Survival, MAP Kinase Signaling System, Breast Neoplasms, Antineoplastic Agents, Phytogenic, Microtubules, Enzyme Activation, Proto-Oncogene Proteins c-raf, Drug Resistance, Neoplasm, Tumor Cells, Cultured, Humans, Hypoglycemic Agents, Insulin, Drug Therapy, Combination, Female, Enzyme Inhibitors, Phosphorylation, Tumor Suppressor Protein p53
Flavonoids, Paclitaxel, Cell Survival, MAP Kinase Signaling System, Breast Neoplasms, Antineoplastic Agents, Phytogenic, Microtubules, Enzyme Activation, Proto-Oncogene Proteins c-raf, Drug Resistance, Neoplasm, Tumor Cells, Cultured, Humans, Hypoglycemic Agents, Insulin, Drug Therapy, Combination, Female, Enzyme Inhibitors, Phosphorylation, Tumor Suppressor Protein p53
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