当前位置: X-MOL 学术Mol. Cancer Res. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Protein Arginine Methyltransferase 5 (PRMT5) and the ERK1/2 & PI3K Pathways: A Case for PRMT5 Inhibition and Combination Therapies in Cancer
Molecular Cancer Research ( IF 4.1 ) Pub Date : 2020-12-07 , DOI: 10.1158/1541-7786.mcr-20-0745
Tzuriel Sapir 1 , David Shifteh 1 , Moshe Pahmer 1 , Sanjay Goel 2 , Radhashree Maitra 1
Affiliation  

The ERK1/2 (RAS, RAF, MEK, ERK) and PI3K (PI3K, AKT, mTOR, PTEN) pathways are the chief signaling pathways for cellular proliferation, survival, and differentiation. Overactivation and hyperphosphorylation of the ERK1/2 & PI3K pathways is frequently observed in cancer and is associated with poor patient prognosis. While it is well known that genetic alterations lead to the dysregulation of the ERK1/2 & PI3K pathways, increasing evidence is showcasing that epigenetic alterations also play a major role in the regulation of the ERK1/2 & PI3K pathways. Protein Arginine Methyltransferase 5 (PRMT5) is a post-translational modifier for multiple cellular processes that is currently being tested as a therapeutic target for cancer. PRMT5 has been shown to be overexpressed in many types of cancers, as well as negatively correlated with patient survival. Numerous studies are indicating that as a post-translational modifier, PRMT5 is extensively involved in regulating the ERK1/2 & PI3K pathways. Additionally, a large number of in vitro and in vivo studies are demonstrating that PRMT5 inhibition, as well as PRMT5 and ERK1/2 & PI3K combination therapies, show significant therapeutic effects in many cancer types. In this review, we explore the vast interactions that PRMT5 has with the ERK1/2 & PI3K pathways, and we make the case for further testing of PRMT5 inhibition, as well as PRMT5 and ERK1/2 & PI3K combination therapies, for the treatment of cancer.

中文翻译:

蛋白质精氨酸甲基转移酶 5 (PRMT5) 和 ERK1/2 和 PI3K 通路:PRMT5 抑制和联合治疗癌症的案例

ERK1/2(RAS、RAF、MEK、ERK)和 PI3K(PI3K、AKT、mTOR、PTEN)通路是细胞增殖、存活和分化的主要信号通路。在癌症中经常观察到 ERK1/2 和 PI3K 通路的过度激活和过度磷酸化,并且与患者预后不良有关。虽然众所周知遗传改变会导致 ERK1/2 和 PI3K 通路的失调,但越来越多的证据表明,表观遗传改变也在 ERK1/2 和 PI3K 通路的调节中发挥重要作用。蛋白质精氨酸甲基转移酶 5 (PRMT5) 是多种细胞过程的翻译后修饰剂,目前正在作为癌症治疗靶点进行测试。PRMT5 已被证明在多种癌症中过度表达,并且与患者生存呈负相关。大量研究表明,作为翻译后修饰剂,PRMT5 广泛参与调节 ERK1/2 和 PI3K 通路。此外,大量体外和体内研究表明,PRMT5 抑制以及 PRMT5 和 ERK1/2 和 PI3K 联合疗法在许多癌症类型中显示出显着的治疗效果。在这篇综述中,我们探讨了 PRMT5 与 ERK1/2 和 PI3K 通路之间的广泛相互作用,并为进一步测试 PRMT5 抑制以及 PRMT5 和 ERK1/2 和 PI3K 联合疗法以治疗癌症。大量体外和体内研究表明,PRMT5 抑制以及 PRMT5 和 ERK1/2 和 PI3K 联合疗法在许多癌症类型中显示出显着的治疗效果。在这篇综述中,我们探讨了 PRMT5 与 ERK1/2 和 PI3K 通路之间的广泛相互作用,并为进一步测试 PRMT5 抑制以及 PRMT5 和 ERK1/2 和 PI3K 联合疗法以治疗癌症。大量体外和体内研究表明,PRMT5 抑制以及 PRMT5 和 ERK1/2 和 PI3K 联合疗法在许多癌症类型中显示出显着的治疗效果。在这篇综述中,我们探讨了 PRMT5 与 ERK1/2 和 PI3K 通路之间的广泛相互作用,并为进一步测试 PRMT5 抑制以及 PRMT5 和 ERK1/2 和 PI3K 联合疗法以治疗癌症。
更新日期:2020-12-07
down
wechat
bug