THE E3 UBIQUITIN LIGASE CBL-B REVERSES MULTIDRUG RESISTANCE OF MCF-7/ADR CELLS THROUGH SUPPRESSION OF PI3K/AKT SIGNALING PATHWAY AND DOWN-REGULATION OF P-GLYCOPROTEIN
Objectives: Following chemotherapy, multidrugresistant (MDR) tumors often emerge, patients with such tumors have a poor prognosis. Clinically applicable regimens for overcoming MDR of different tumors are not yet available. Some studies have shown that inhibition of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway can reverse P-gpmediated MDR in some cancer cells. The Casitas B cell lymphoma-b (Cbl-b) proto-oncogene is an E3 ubiquitin ligase that regulates the ubiquitination and proteasome-dependent degradation of a number of proteins. In previous studies, we reported a substantial downregulation of Cbl-b in the MDR gastric carcinoma cell lines compared with parental cell lines. Overexpression of Cbl-b has also been shown to sensitize MDR cells to chemotherapeutic agents, such as adriamycin and vincristine. However, the mechanism of Cbl-b involved breast cancer MDR through inhibition of PI3K/Akt signaling pathway is unclear.
Ye Zhang Xiujuan Qu Xuejun Hu Xianghong Yang Kezuo Hou Yuee Teng Jingdong Zhang Yunpeng Liu
Department of Medical Oncology, the First Hospital of China Medical University, Shenyang 110001, Chi 2 Department of Medical Respiratory, the First Hospital, China Medical University,Shenyang, 110001, Department of Pathology, the Shengjing Hospital of China Medical University, Shenyang 110004, China
国际会议
亚太地区国际肿瘤生物学和医学学术会议、全国肿瘤标志学术大会、第六届中国中青年肿瘤专家论坛
上海
英文
400-401
2011-10-13（万方平台首次上网日期，不代表论文的发表时间）