Hematology, Oncology and Stem Cell Transplantation Research Center, Shariati Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Department of Medical Oncology and Hematology, Iran University of Medical Sciences, Tehran, Iran.
Mol Biol Rep. 2021 Dec;48(12):8045-8059. doi: 10.1007/s11033-021-06739-6. Epub 2021 Oct 23.
Along with evolution, a considerable number of signaling cascades have evolved within cells to meet their multifaceted needs. Among transmitting molecules, phosphoinositide 3-kinase (PI3K), Akt, and mammalian target of rapamycin (mTOR) have teamed up to build a signaling axis that effectively regulates various cellular processes including cell proliferation and migration. Given the extensive output of the PI3K/Akt/mTOR signaling axis, its aberrancy could subsequently lead to the formation of a wide range of human cancers spanning from hematologic malignancies to different types of solid tumors. Despite the high frequency of the PI3K pathway over-activation in most malignancies, mutations in the DNA sequence are not equally common. Such incompatibility sheds light on the possible effects of post-translational modification mechanisms that may take control of this pathway, some of the most important ones of which are through microRNAs (miRNAs or miRs). The present review is designed to take off the veil from the regulatory role of these small non-coding RNAs on the PI3K/Akt/mTOR signaling axis in carcinogenesis.
随着进化，细胞内已经进化出相当数量的信号级联来满足它们多方面的需求。在传递分子中，磷酸肌醇 3-激酶 (PI3K)、Akt 和雷帕霉素靶蛋白 (mTOR) 已经联手构建了一个信号轴，有效地调节包括细胞增殖和迁移在内的各种细胞过程。鉴于 PI3K/Akt/mTOR 信号轴的广泛输出，如果其异常，可能会导致从血液恶性肿瘤到不同类型实体瘤的广泛人类癌症的形成。尽管在大多数恶性肿瘤中，PI3K 途径的过度激活频率很高，但 DNA 序列中的突变并不常见。这种不兼容性表明可能存在翻译后修饰机制的影响，这些机制可能控制着该途径，其中一些最重要的机制是通过 microRNAs（miRNAs 或 miRs）。本综述旨在揭示这些小分子非编码 RNA 在致癌作用中对 PI3K/Akt/mTOR 信号轴的调节作用。
