Quan Zihan, Yang Yang, Zheng Hongmei, Zhan Yuting, Luo Jiadi, Ning Yue, Fan Songqing
Department of Pathology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
J Cancer. 2022 Oct 3;13(13):3434-3443. doi: 10.7150/jca.77619. eCollection 2022.
The discovery of immune checkpoints has been well known to provide novel clues for cancer treatments. Immunotherapy against the programmed cell death protein-1 (PD-1) /programmed death-ligand-1 (PD-L1), one of the most popular auxiliary treatments in recent years, has been applied in various tumor treatments, including non-small cell lung cancer (NSCLC). However, inevitable issues such as side effects and drug resistance emerge following the use of immune checkpoint inhibitors. The PI3K/AKT/mTOR pathway may participate in the regulation of PD-L1 expression. Abnormal PI3K/AKT/mTOR pathway activation results in increased PD-L1 protein translation, whereas PD-L1 overexpression can activate the PI3K/AKT/mTOR pathway inversely. Via downstream proteins, including 4E-BP1, STAT3, NF-κB, c-MYC, and AMPK in aberrant energy status, the PI3K/AKT/mTOR pathway can regulate PD-L1 post-transcription and translation. Besides, the regulation of the PI3K pathway by the PD-1/PD-L1 axis involves both tumor cells and the tumor immune microenvironment. Inhibitors targeting the PD-1/PD-L1 have been successfully applied in the treatment of gastrointestinal cancer and breast cancer. Meanwhile, drug resistance from alternative pathway activation also evidently affects clinical progress. To achieve a better therapeutic effect and quality of survival, the combination of multiple treatment modalities presents great research value. Here we reviewed the interaction between PD-1/PD-L1 and PI3K/AKT/mTOR pathway in the progression and treatment of NSCLC and summarized its clinical implications. The intracellular interactions between PD-1/PD-L1 and the PI3K/AKT/mTOR pathway indicate that PD-1/PD-L1 inhibitors have a wide range of potential applications. And we presented the mechanism for combining therapy with monoclonal antibody PD-1/PD-L1 and PI3K/AKT/mTOR inhibitors in this review, to broaden the therapies for NSCLC.
免疫检查点的发现为癌症治疗提供了新线索,这已广为人知。针对程序性细胞死亡蛋白1(PD-1)/程序性死亡配体1(PD-L1)的免疫疗法是近年来最流行的辅助治疗方法之一,已应用于包括非小细胞肺癌(NSCLC)在内的各种肿瘤治疗中。然而,使用免疫检查点抑制剂后会出现诸如副作用和耐药性等不可避免的问题。PI3K/AKT/mTOR通路可能参与PD-L1表达的调控。PI3K/AKT/mTOR通路的异常激活会导致PD-L1蛋白翻译增加,而PD-L1的过表达则会反向激活PI3K/AKT/mTOR通路。通过下游蛋白,包括能量状态异常时的4E-BP1、STAT3、NF-κB、c-MYC和AMPK,PI3K/AKT/mTOR通路可以调节PD-L1的转录后和翻译过程。此外,PD-1/PD-L1轴对PI3K通路的调节涉及肿瘤细胞和肿瘤免疫微环境。靶向PD-1/PD-L1的抑制剂已成功应用于胃肠道癌和乳腺癌的治疗。同时,替代通路激活导致的耐药性也明显影响临床进展。为了获得更好的治疗效果和生存质量,多种治疗方式的联合具有很大的研究价值。在此,我们综述了PD-1/PD-L1与PI3K/AKT/mTOR通路在NSCLC进展和治疗中的相互作用,并总结了其临床意义。PD-1/PD-L1与PI3K/AKT/mTOR通路之间的细胞内相互作用表明,PD-1/PD-L1抑制剂具有广泛的潜在应用。在本综述中,我们阐述了单克隆抗体PD-1/PD-L1与PI3K/AKT/mTOR抑制剂联合治疗的机制,以拓宽NSCLC的治疗方法。