Downregulation of miR-21 as a promising strategy to overcome drug resistance in cancer

Enhanced theranostic efficacy of epirubicin-loaded SPION@MSN through co-delivery of an anti-miR-21-expressing plasmid and ZIF-8 hybridization to target colon adenocarcinoma

“…56 Studies have demonstrated that the inhibition of miR-21 can reverse the suppression of cell death and enhance the response to chemotherapeutic drugs. 11,57 Therefore, a practical approach for synergistic cancer treatment could involve the co-delivery of chemotherapeutic drugs like EPI along with anti-miR-21-expressing plasmids via biocompatible nanoparticles such as MSNs. 55,58 In this research, the characteristics of SPION@MSN-based nanoparticles were investigated using physical and chemical methods.…”

“…10 Various blocking methods, including anti-miRNAs, miRNA sponges, miRNA masking, and small enabler molecules, have been used effectively to hinder the function of cancer-causing miRNAs like miR-21. 11 Among the various strategies employed in miRNA-based cancer therapy, using lentiviral plasmids expressing anti-miRNAs has gained recognition as an effective approach. 12 However, limited research has explored the potential of pmiRZIP-21, a lentiviral plasmid expressing anti-miR-21, in combination with co-delivery of chemotherapeutic drugs.…”

Shikonin Causes an Apoptotic Effect on Human Kidney Cancer Cells through Ras/MAPK and PI3K/AKT Pathways

“…MicroRNA-21 is involved in all the carcinogenesis phases, including initiation, promotion, progression, and metastasis. Studies have shown that upregulated miR-21 can induce Reactive Oxygen Species (ROS) production through the MAPK signaling pathway and is involved in the development of resistance to chemotherapeutic agents [ 47 ].…”

Cancer cell cycle heterogeneity as a critical determinant of therapeutic resistance

“… 52 Acquired resistance can be identified by the gradual reduction of the anticancer efficacy of a drug following the treatment. 51 This phenomenon can be the outcome of various cellular and molecular responses, including (1) activation of a second proto-oncogene that becomes the newly emerged driver gene; cancer cells can acquire resistance against targeted drugs by the generation of new mutations or alteration in the expression; (2) alterations in expression levels of the drug targets; (3) change in drug metabolism in the tumor cells; (4) upregulation of transmembrane transporters which efflux the drugs; (5) epigenomic changes and altered levels of microRNAs, 53 which lead to variations in the downstream or upstream receptors; and (6) changes in tumor microenvironment after treatment. Therefore, it can be concluded that the “resistant populations” of neoplastic cells by using various underlying mechanisms, which are well described in a review by Haider et al, lead to chemotherapy failure in cancer.…”