Sun Shi-Yong
Department of Hematology and Medical Oncology, Emory University of School of Medicine, Winship Cancer Institute of Emory University, Atlanta, GA, United States of America.
Transl Oncol. 2020 Dec;13(12):100847. doi: 10.1016/j.tranon.2020.100847. Epub 2020 Aug 24.
The mammalian target of rapamycin (mTOR), via forming two important complexes: mTOR complex 1 (mTORC1) and complex 2 (mTORC2), plays an important role in the regulation of immunity in addition to exerting many other biological funcions. Beyond its regulatory effects on immune cells, the mTOR axis also regulates the expression of programmed death-ligand 1 (PD-L1) in cancer cells; accordingly, inhibition of mTOR alters PD-L1 levels in different cancer cell types. However, the currently published studies on mTOR inhibition-induced PD-L1 alteration have generated conflicting results. This review will focus on summarizing current findings in this regard and discussing possible reasons for the discrepancies and their potential implications for PD-L1 modulation in cancer therapy.
雷帕霉素的哺乳动物靶点(mTOR)通过形成两种重要复合物:mTOR复合物1(mTORC1)和复合物2(mTORC2),除发挥许多其他生物学功能外,在免疫调节中也起着重要作用。除了对免疫细胞的调节作用外,mTOR轴还调节癌细胞中程序性死亡配体1(PD-L1)的表达;因此,抑制mTOR会改变不同癌细胞类型中PD-L1的水平。然而,目前已发表的关于mTOR抑制诱导的PD-L1改变的研究结果相互矛盾。本综述将重点总结这方面的当前研究结果,并讨论差异产生的可能原因及其对癌症治疗中PD-L1调节的潜在影响。