自噬
小RNA
癌症研究
生物
癌症
癌细胞
癌基因
表观遗传学
抑制器
细胞生物学
细胞凋亡
细胞周期
基因
遗传学
作者
Milad Ashrafizadeh,Ali Zarrabi,Sima Orouei,Kiavash Hushmandi,Azadeh Hakimi,Amirhossein Zabolian,Salman Daneshi,Saeed Samarghandian,Behzad Baradaran,Masoud Najafi
标识
DOI:10.1016/j.ejphar.2020.173660
摘要
Chemoresistance has doubled the effort needed to reach an effective treatment for cancer. Now, scientists should consider molecular pathways and mechanisms involved in chemoresistance to overcome cancer. Autophagy is a “self-digestion” mechanism in which potentially toxic and aged organelles and macromolecules are degraded. Increasing evidence has shown that autophagy possesses dual role in cancer cells (onco-suppressor or oncogene). So, it is vital to identify its role in cancer progression and malignancy. MicroRNAs (miRs) are epigenetic factors capable of modulation of autophagy in cancer cells. In the current review, we emphasize on the relationship between miRs and autophagy in cancer chemotherapy. Besides, we discuss upstream mediators of miR/autophagy axis in cancer chemotherapy including long non-coding RNAs, circular RNAs, Nrf2 c-Myc, and HIF-1α. At the final section, we provide a discussion about how anti-tumor compounds affect miR/autophagy axis in ensuring chemosensitivity. These topics are described in this review to show how autophagy inhibition/induction can lead to chemosensitivity/chemoresistance, and miRs are considered as key players in these discussions. • Autophagy is a “self-digestion” process with involvement in cancer inhibition/progression. • MicroRNAs (miRs) as regulator of biological processes, regulate autophagy in cancer cells. • Autophagy regulation by miRs is of importance in chemoresistance/chemosensitivity. • Other molecular pathways such as lncRNAs, circRNAs, Nrf2 and c-Myc can regulate miR/autophagy axis in chemotherapy. • Anti-tumor compounds regulate miR/autophagy axis in promoting efficacy of chemotherapy in cancer therapy.
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