Tolue Ghasaban Faezeh, Maharati Amirhosein, Akhlaghipour Iman, Moghbeli Meysam
Department of Medical Genetics and Molecular Medicine, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Student Research Committee, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Cancer Cell Int. 2023 Apr 25;23(1):80. doi: 10.1186/s12935-023-02925-7.
Chemotherapy is one of the most common therapeutic methods in advanced and metastatic tumors. Cisplatin (CDDP) is considered as one of the main first-line chemotherapy drugs in solid tumors. However, there is a high rate of CDDP resistance in cancer patients. Multi-drug resistance (MDR) as one of the main therapeutic challenges in cancer patients is associated with various cellular processes such as drug efflux, DNA repair, and autophagy. Autophagy is a cellular mechanism that protects the tumor cells toward the chemotherapeutic drugs. Therefore, autophagy regulatory factors can increase or decrease the chemotherapy response in tumor cells. MicroRNAs (miRNAs) have a pivotal role in regulation of autophagy in normal and tumor cells. Therefore, in the present review, we discussed the role of miRNAs in CDDP response through the regulation of autophagy. It has been reported that miRNAs mainly increased the CDDP sensitivity in tumor cells by inhibition of autophagy. PI3K/AKT signaling pathway and autophagy-related genes (ATGs) were the main targets of miRNAs in the regulation of autophagy-mediated CDDP response in tumor cells. This review can be an effective step to introduce the miRNAs as efficient therapeutic options to increase autophagy-mediated CDDP sensitivity in tumor cells.
化疗是晚期和转移性肿瘤最常见的治疗方法之一。顺铂（CDDP）被认为是实体瘤主要的一线化疗药物之一。然而，癌症患者中CDDP耐药率很高。多药耐药（MDR）作为癌症患者主要的治疗挑战之一，与多种细胞过程相关，如药物外排、DNA修复和自噬。自噬是一种保护肿瘤细胞免受化疗药物作用的细胞机制。因此，自噬调节因子可增加或降低肿瘤细胞的化疗反应。微小RNA（miRNA）在正常细胞和肿瘤细胞的自噬调节中起关键作用。因此，在本综述中，我们讨论了miRNA通过调节自噬在CDDP反应中的作用。据报道，miRNA主要通过抑制自噬增加肿瘤细胞对CDDP的敏感性。PI3K/AKT信号通路和自噬相关基因（ATG）是miRNA在调节肿瘤细胞自噬介导的CDDP反应中的主要靶点。本综述可为将miRNA作为增加肿瘤细胞自噬介导的CDDP敏感性的有效治疗选择提供有效途径。
