Chang Insoon, Loo Yi-Ling, Patel Jay, Nguyen Joe Truong, Kim Jin Koo, Krebsbach Paul H
Section of Endodontics, Division of Regenerative and Reconstructive Sciences, School of Dentistry, University of California, Los Angeles, Los Angeles, CA, United States.
School of Dentistry, University of California, Los Angeles, Los Angeles, CA, United States.
Front Oncol. 2024 Mar 12;14:1375498. doi: 10.3389/fonc.2024.1375498. eCollection 2024.
mEAK-7 (mammalian EAK-7 or MTOR-associated protein, eak-7 homolog), is an evolutionarily conserved lysosomal membrane protein that is highly expressed in several cancer cells. Multiple recent studies have identified mEAK-7 as a positive activator of mTOR (mammalian/mechanistic target of rapamycin) signaling via an alternative mTOR complex, implying that mEAK-7 plays an important role in the promotion of cancer proliferation and migration. In addition, structural analyses investigating interactions between mEAK-7 and V-ATPase, a protein complex responsible for regulating pH homeostasis in cellular compartments, have suggested that mEAK-7 may contribute to V-ATPase-mediated mTORC1 activation. The C-terminal α-helix of mEAK-7 binds to the D and B subunits of the V-ATPase, creating a pincer-like grip around its B subunit. This binding undergoes partial disruption during ATP hydrolysis, potentially enabling other proteins such as mTOR to bind to the α-helix of mEAK-7. mEAK-7 also promotes chemoresistance and radiation resistance by sustaining DNA damage-mediated mTOR signaling through interactions with DNA-PKcs (DNA-dependent protein kinase catalytic subunit). Taken together, these findings indicate that mEAK-7 may be a promising therapeutic target against tumors. However, the precise molecular mechanisms and signal transduction pathways of mEAK-7 in cancer remain largely unknown, motivating the need for further investigation. Here, we summarize the current known roles of mEAK-7 in normal physiology and cancer development by reviewing the latest studies and discuss potential future developments of mEAK-7 in targeted cancer therapy.
mEAK-7(哺乳动物EAK-7或与mTOR相关的蛋白,eak-7同源物)是一种在进化上保守的溶酶体膜蛋白,在多种癌细胞中高度表达。最近的多项研究已将mEAK-7鉴定为通过一种替代性mTOR复合物对mTOR(哺乳动物雷帕霉素靶蛋白/机制性雷帕霉素靶蛋白)信号传导的正向激活剂,这意味着mEAK-7在促进癌症增殖和迁移中起重要作用。此外,对mEAK-7与V-ATP酶(一种负责调节细胞内区室pH稳态的蛋白复合物)之间相互作用的结构分析表明,mEAK-7可能有助于V-ATP酶介导的mTORC1激活。mEAK-7的C末端α螺旋与V-ATP酶的D和B亚基结合,在其B亚基周围形成钳状抓握。这种结合在ATP水解过程中会部分破坏,可能使其他蛋白(如mTOR)能够与mEAK-7的α螺旋结合。mEAK-7还通过与DNA-PKcs(DNA依赖性蛋白激酶催化亚基)相互作用维持DNA损伤介导的mTOR信号传导,从而促进化学抗性和辐射抗性。综上所述,这些发现表明mEAK-7可能是一种有前景的肿瘤治疗靶点。然而,mEAK-7在癌症中的精确分子机制和信号转导途径仍 largely未知,这激发了进一步研究的必要性。在此,我们通过综述最新研究总结了mEAK-7在正常生理和癌症发展中的当前已知作用,并讨论了mEAK-7在靶向癌症治疗中的潜在未来发展。