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CLIP-170 Mediates Paclitaxel Sensitivity in Breast Cancer

Expression tied to pathologic response; induces mitotic arrest, apoptosis, microtubule assembly

FRIDAY, Oct. 21 (HealthDay News) -- CLIP-170 regulates paclitaxel sensitivity in breast cancer cells by mediating the effects of paclitaxel on microtubule assembly, mitosis, and apoptosis, according to a study published online Oct. 12 in The Journal of Pathology.

Xiaodong Sun, from the Nankai University in Tianjin, China, and colleagues investigated whether the microtubule binding protein CLIP-170 regulated sensitivity of the anti-microtubule drug paclitaxel in tumor samples from 63 breast cancer patients who were treated with sequential weekly paclitaxel followed by 5-fluorouracil, doxorubicin, and cyclophosphamide. Samples were obtained by surgical resection, following three courses of chemotherapy. Pathologic response was assessed by a pathologist, and was defined by the proportion of histologic changes in surgical specimens. The effect of paclitaxel on cell proliferation in vitro was examined, and mitotic index and caspase-3 activity were assessed.

The investigators found that the pathologic response of tumors to paclitaxel-containing chemotherapy correlated with CLIP-170 expression in clinical samples of breast cancer. Expression of CLIP-170 increased the ability of paclitaxel to induce apoptosis and inhibit cell cycle progression at mitosis in breast cancer cells. CLIP-170 promoted paclitaxel binding to microtubules and enhanced paclitaxel activity in promoting microtubule assembly.

"These results demonstrate that CLIP-170 mediates paclitaxel sensitivity in breast cancer via a microtubule-dependent mechanism," the authors write.

Abstract
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