Basu Alakananda, Sivaprasad Usha
Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Cell Signal. 2007 Aug;19(8):1633-42. doi: 10.1016/j.cellsig.2007.04.008. Epub 2007 May 1.
Cancer is caused by dysregulation in cellular signaling systems that control cell proliferation, differentiation and cell death. Protein kinase C (PKC), a family of serine/threonine kinases, plays an important role in the growth factor signal transduction pathway. PKCepsilon, however, is the only PKCepsilon isozyme that has been considered as an oncogene. It can contribute to malignancy by enhancing cell proliferation or by inhibiting cell death. This review focuses on how PKCepsilon collaborates with other signaling pathways, such as Ras/Raf/ERK and Akt, to regulate cell survival and cell death. We have also discussed how PKCepsilon mediates its antiapoptotic signal by altering the level or function of pro- and antiapoptotic Bcl-2 family members.
癌症是由控制细胞增殖、分化和细胞死亡的细胞信号系统失调引起的。蛋白激酶C（PKC）是丝氨酸/苏氨酸激酶家族，在生长因子信号转导通路中起重要作用。然而，PKCε是唯一被认为是癌基因的PKC同工酶。它可通过增强细胞增殖或抑制细胞死亡导致恶性肿瘤。本综述重点关注PKCε如何与其他信号通路（如Ras/Raf/ERK和Akt）协同作用来调节细胞存活和细胞死亡。我们还讨论了PKCε如何通过改变促凋亡和抗凋亡Bcl-2家族成员的水平或功能来介导其抗凋亡信号。
