CD133 suppression increases the sensitivity of prostate cancer cells to paclitaxel.

摘要: One of the major barriers in cancer therapy is resistance to conventional therapies and stem cells (CSCs) are among main causes this problem. CD133 as a CSC marker displays cell-like properties, tumorigenic capacity, drug various cancers. However, molecular mechanism behind function prostate (PC) still remains unclear. This research aimed illustrate probabilistic CD133-siRNA paclitaxel reduction chemoresistance PC cells. To measure cell viability, migratory CSCs invasive potential, apoptosis cycle progression cells, MTT, wound healing, spheroid assay, colony formation DAPI staining flow cytometry assays were applied LNCaP line, respectively. Also, quantitative real-time PCR (qRT-PCR) western blot method used for measuring expression effects silencing on AKT/mTOR/c-myc axis pro-metastatic genes expression. We showed that considerably decreased Moreover, treatment significantly proliferation also inhibited ability migration invasion reduced Additionally, we found simultaneous use increased paclitaxel-induced apoptosis. Our results confirmed combined with synergistically could suppress migration, invasion, enhance chemosensitivity compared mono treatment. Therefore, be viewed promising efficient strategy targeted therapies.