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
Full Text (subscription or payment may be required)

Physician's Briefing

Updated on June 05, 2022

Read this Next
About UsOur ProductsCustom SolutionsHow it’s SoldOur ResultsDeliveryContact UsBlogPrivacy PolicyFAQ