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δ-Catenin Participates in EGF/AKT/p21Waf Signaling and Induces Prostate Cancer Cell Proliferation and Invasion
Authors:Yingjie Shen  Hyoung Jae Lee  Rui Zhou  Hangun Kim  Gen Chen  Young-Chang Cho  Kwonseop Kim
Affiliation:1.College of Pharmacy and Research Institute of Pharmaceutical Sciences, Chonnam National University, Gwangju 61186, Korea; (Y.S.); (H.J.L.); (G.C.); (Y.-C.C.);2.College of Pharmacy and Research Institute of Life and Pharmaceutical Sciences, Sunchon National University, Sunchon 57922, Korea; (R.Z.); (H.K.)
Abstract:Prostate cancer (PCa) is the second most leading cause of death in males. Our previous studies have demonstrated that δ-catenin plays an important role in prostate cancer progression. However, the molecular mechanism underlying the regulation of δ-catenin has not been fully explored yet. In the present study, we found that δ-catenin could induce phosphorylation of p21Waf and stabilize p21 in the cytoplasm, thus blocking its nuclear accumulation for the first time. We also found that δ-catenin could regulate the interaction between AKT and p21, leading to phosphorylation of p21 at Thr-145 residue. Finally, EGF was found to be a key factor upstream of AKT/δ-catenin/p21 for promoting proliferation and metastasis in prostate cancer. Our findings provide new insights into molecular controls of EGF and the development of potential therapeutics targeting δ-catenin to control prostate cancer progression.
Keywords:δ  -catenin, prostate cancer, EGF, AKT, p21Waf
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