Faculty of Engineering and Natural Sciences, Sabanci University, Orta Mahalle, Üniversite Caddesi No. 27, Orhanlı, Tuzla, 34956, Istanbul, Turkey.
Department of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
J Exp Clin Cancer Res. 2022 Mar 22;41(1):105. doi: 10.1186/s13046-022-02293-6.
Prostate cancer is a leading cause of death worldwide and new estimates revealed prostate cancer as the leading cause of death in men in 2021. Therefore, new strategies are pertinent in the treatment of this malignant disease. Macroautophagy/autophagy is a "self-degradation" mechanism capable of facilitating the turnover of long-lived and toxic macromolecules and organelles. Recently, attention has been drawn towards the role of autophagy in cancer and how its modulation provides effective cancer therapy. In the present review, we provide a mechanistic discussion of autophagy in prostate cancer. Autophagy can promote/inhibit proliferation and survival of prostate cancer cells. Besides, metastasis of prostate cancer cells is affected (via induction and inhibition) by autophagy. Autophagy can affect the response of prostate cancer cells to therapy such as chemotherapy and radiotherapy, given the close association between autophagy and apoptosis. Increasing evidence has demonstrated that upstream mediators such as AMPK, non-coding RNAs, KLF5, MTOR and others regulate autophagy in prostate cancer. Anti-tumor compounds, for instance phytochemicals, dually inhibit or induce autophagy in prostate cancer therapy. For improving prostate cancer therapy, nanotherapeutics such as chitosan nanoparticles have been developed. With respect to the context-dependent role of autophagy in prostate cancer, genetic tools such as siRNA and CRISPR-Cas9 can be utilized for targeting autophagic genes. Finally, these findings can be translated into preclinical and clinical studies to improve survival and prognosis of prostate cancer patients.
前列腺癌是全球主要的死亡原因，新的估计显示，前列腺癌是 2021 年男性死亡的主要原因。因此，新的治疗策略对于治疗这种恶性疾病至关重要。自噬是一种“自我降解”的机制，能够促进长寿命和有毒的大分子和细胞器的周转。最近，人们开始关注自噬在癌症中的作用以及其调节如何为癌症治疗提供有效的方法。在本综述中，我们提供了一个关于前列腺癌中自噬的机制讨论。自噬可以促进/抑制前列腺癌细胞的增殖和存活。此外，自噬还可以影响前列腺癌细胞的转移（通过诱导和抑制）。自噬可以影响前列腺癌细胞对化疗和放疗等治疗的反应，因为自噬与细胞凋亡密切相关。越来越多的证据表明，上游调节因子如 AMPK、非编码 RNA、KLF5、MTOR 等调节前列腺癌中的自噬。抗肿瘤化合物，如植物化学物质，在前列腺癌治疗中双重抑制或诱导自噬。为了改善前列腺癌的治疗，已经开发了壳聚糖纳米粒子等纳米治疗方法。鉴于自噬在前列腺癌中的上下文相关作用，可以利用基因工具，如 siRNA 和 CRISPR-Cas9，来靶向自噬基因。最后，这些发现可以转化为临床前和临床研究，以提高前列腺癌患者的生存率和预后。
