Abstract
Centrosome aberrations have been implicated in the development and progression of breast cancer. Our previous worked show that centrosomal protein 70 (Cep70) regulates breast cancer growth and metastasis. However, it remains elusive whether Cep70 is implicated in the sensitivity of the anti-microtubule drug paclitaxel in breast cancer. Here we provide evidence that Cep70 is a mediator of paclitaxel sensitivity in breast cancer. Cell proliferation assays show that Cep70 expression correlates with paclitaxel sensitivity in breast cancer cell lines. In addition, paclitaxel sensitivity varies when altering Cep70 expression level. Mechanistic studies reveal that Cep70 interacts with tubulin, and promotes the ability of paclitaxel to stimulate microtubule assembly. These data demonstrate that Cep70 mediates paclitaxel sensitivity in breast cancer.
Highlights
Breast cancer is the most frequently diagnosed cancer and the leading cause of cancer death in women worldwide [1]
Paclitaxel sensitivity can vary3boef t9ween cancer lines for reasons not fully understood, these results suggest that centrosomal protein 70 (Cep70) expression level may be a factpcoaarnciclnietratxhlieneleisnsefbnorsreiatriesvtaisctoaynntcsoenrpoctaecfllulsilt(layr x=ue−nl0di.n8e5rbs1tr,oepoa=ds0,t .tc0ha3en1s)ec. eArrelstcuheolltlussg.shugpgaecslittathxaetl sensitivity can vary between Cep70 expression level may
Our findings demonstrate that Cep70 modulates the sensitivity of breast cancer cells to paclitaxel
Summary
Breast cancer is the most frequently diagnosed cancer and the leading cause of cancer death in women worldwide [1]. With the development of various therapeutic methods, including surgical resection, radiotherapy, and chemotherapy, the outcomes in breast cancer patients have improved in recent decades [2,3]. Paclitaxel, one of the most effective chemotherapy drugs that stabilizes microtubules, has been widely used to treat various cancers [4,5]. Its effectiveness has been seriously limited by the acquired resistance or variable sensitivity of cancer cells [6]. No predictive marker exists due to the limited knowledge about the mechanism governing paclitaxel sensitivity. There is an urgent need to explore the mechanism underlying the modulation of paclitaxel sensitivity, which will help to improve response rates and potentially extend survival in these patients
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