Department of Molecular Biology & Genetics, Faculty of Science & Letters, Pamukkale University, Denizli, Turkey.
Future Oncol. 2019 Jan;15(1):95-102. doi: 10.2217/fon-2018-0332. Epub 2018 Nov 1.
S6K2, the newer member of S6 Kinase family, is a crucial modulator of Akt/mTOR signaling pathway and is a member of AGC kinase family that regulates cellular growth and survival. S6K1 and S6K2 share high sequence similarity; therefore, S6K2 had been underestimated. However, recent studies displayed distinct functions of S6K2. Activated by both Akt/mTOR and Ras/Raf/Mek/Erk signaling pathways, S6K2 regulates cancer cell survival via different routes. Complexation with antiapoptotic proteins BRAF and PKCε avoids non-small-cell lung cancer cells from apoptosis upon FGF-2 stimulation. Indirect upregulation of the translation of antiapoptotic proteins Bcl-XL and XIAP in HEK293T cells and interference with TNF-induced apoptosis in MCF-7 cells are other routes of cancer cell survival. The aforementioned studies on S6K2 necessitate the development of therapies targeting only on S6K2. Studies targeting S6K2 may help to build important roads for cancer therapy.
S6K2 是 S6 激酶家族的新成员，是 Akt/mTOR 信号通路的关键调节因子，属于 AGC 激酶家族，可调节细胞生长和存活。S6K1 和 S6K2 具有高度的序列相似性；因此，S6K2 一直被低估。然而，最近的研究显示了 S6K2 的不同功能。S6K2 通过 Akt/mTOR 和 Ras/Raf/Mek/Erk 信号通路激活，通过不同途径调节癌细胞存活。与抗凋亡蛋白 BRAF 和 PKCε 形成复合物可防止非小细胞肺癌细胞在 FGF-2 刺激下发生凋亡。在 HEK293T 细胞中间接上调抗凋亡蛋白 Bcl-XL 和 XIAP 的翻译以及干扰 MCF-7 细胞中 TNF 诱导的细胞凋亡是癌细胞存活的其他途径。上述关于 S6K2 的研究需要开发仅针对 S6K2 的治疗方法。针对 S6K2 的研究可能有助于为癌症治疗开辟重要道路。
