研究动态
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miRNA 在阿霉素耐药中的调节作用:机制观点。

Modulatory effects of miRNAs in doxorubicin resistance: A mechanistic view.

发表日期:2024 Sep 02
作者: Fatemeh Ebadi Meinag, Mina Fatahi, Vahid Vahedian, Nazila Fathi Maroufi, Bashir Mosayyebi, Elham Ahmadi, Mohammad Rahmati
来源: Cellular & Molecular Immunology

摘要:

MicroRNA(miRNA)是一类小非编码RNA,在细胞周期控制、凋亡、代谢、发育和分化等重要生物过程中发挥着重要作用,导致神经、代谢紊乱、和癌症。化疗被认为是癌症患者的黄金治疗方法。然而,化疗是癌症管理的主要挑战之一。阿霉素 (DOX) 是一种抗癌药物,可干扰癌细胞的生长和扩散。 DOX 用于治疗各种类型的癌症,包括乳腺癌、神经组织癌、膀胱癌、胃癌、卵巢癌、甲状腺癌、肺癌、骨癌、肌肉癌、关节癌和软组织癌。最近,miRNA 被确定为特定基因的主要调节因子,负责启动化学抗性的机制。 miRNA通过调节细胞凋亡过程对化疗耐药发挥调节作用。此外,研究还证实了 miRNA p53 基因作为关键肿瘤抑制因子的作用。 miRNA可以影响主要的生物通路,包括PI3K通路。本综述旨在介绍目前对 miRNA 对细胞凋亡、p53 和与 DOX 耐药相关的 PTEN/PI3K/Akt 信号通路的影响的机制和影响的理解。© 2024。作者,获得 Springer-Verlag GmbH 德国的独家许可,施普林格自然的一部分。
MicroRNAs (miRNAs) are a group of small non-coding RNAs and play an important role in controlling vital biological processes, including cell cycle control, apoptosis, metabolism, and development and differentiation, which lead to various diseases such as neurological, metabolic disorders, and cancer. Chemotherapy consider as gold treatment approaches for cancer patients. However, chemotherapeutic is one of the main challenges in cancer management. Doxorubicin (DOX) is an anti-cancer drug that interferes with the growth and spread of cancer cells. DOX is used to treat various types of cancer, including breast, nervous tissue, bladder, stomach, ovary, thyroid, lung, bone, muscle, joint and soft tissue cancers. Also recently, miRNAs have been identified as master regulators of specific genes responsible for the mechanisms that initiate chemical resistance. miRNAs have a regulatory effect on chemotherapy resistance through the regulation of apoptosis process. Also, the effect of miRNAs p53 gene as a key tumor suppressor was confirmed via studies. miRNAs can affect main biological pathways include PI3K pathway. This review aimed to present the current understanding of the mechanisms and effects of miRNAs on apoptosis, p53 and PTEN/PI3K/Akt signaling pathway related to DOX resistance.© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.