CD44 regulates prostate cancer proliferation, invasion and migration via PDK1 and PFKFB4
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Wei Li1,*, Li Qian2,*, Junhao Lin1, Guihai Huang1, Nan Hao1, Xiuwang Wei1, Wei Wang1 and Jianbo Liang1
1Department of Urology, The People’s Hospital of Guangxi Zhuang Autonomous Region, NanNing, China
2Department of Pharmacy, The People’s Hospital of Guangxi Zhuang Autonomous Region, NanNing, China
*These authors have contributed equally to this work
Wei Li, email: firstname.lastname@example.org
Keywords: prostate cancer, CD44, PDK1, PFKFB4, metabolism
Received: February 04, 2017 Accepted: April 05, 2017 Published: May 11, 2017
Our recent studies have shown that CD44, a cell-surface protein with functions in many biologic processes, involved in glucose metabolism of prostate cancer cells. However, the molecular mechanisms of the regulation need to be further elucidated. In present study, LNCaP cells infected with lentivirus vector overexpressing CD44. The expression levels of key enzymes in glucose metabolism known as PDK1 and PFKFB4 were determined using QRT-PCR and western blot. PDK1 and PFKFB4 in LNCaP and PC3 cells were knocked down with shRNA respectively, and then cell proliferation, invasion and cell migration assay were performed. We found that overexpression of CD44 increased expression levels of PDK1 and PFKFB4 in LNCaP cells. Silencing of PDK1 and PFKFB4 could decrease cell proliferation, inhibit invasion and migration ability of prostate cancer cells. In addition, CD44 inhibitor could decrease glucose consumption and increase ROS levels of PC-3 cells significantly, as well as sensitize PC-3 cells to docetaxel. Taken together, CD44 could modulate aggressive phenotype of prostate cancer cells, by regulation of the expression of PDK1 and PFKFB4. CD44 may be a novel potential therapeutic target.
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