Мақола

miR-155 and the orchestration of cell-death evasion and chemoresistance in cancer: Isoform-specific mechanisms and therapeutic opportunities

Saeb Abdul-RahmanDepartment of Anesthesia Techniques, health and medical techniques college, Alnoor University, Mosul, Iraq. Electronic address: [email protected]Abdulkareem ShareefAhl al bayt University, Kerbala, Iraq. Electronic address: [email protected]S. Renuka JyothiDepartment of Biotechnology and Genetics, School of Sciences, JAIN (Deemed to be University), Bangalore, Karnataka, India. Electronic address: [email protected]Priya Priyadarshini NayakDepartment of Medical Oncology, IMS and SUM Hospital, Siksha 'O' Anusandhan (Deemed to be University), Bhubaneswar, Odisha 751003, India. Electronic address: [email protected]J. Bethanney JanneyDepartment of Biomedical, Sathyabama Institute of Science and Technology, Chennai, Tamil Nadu, India. Electronic address: [email protected]Gurjant SinghDepartment of Physiotherapy, University Institute of Allied Health Sciences, Chandigarh University, Chandigarh State, Punjab, India. Electronic address: [email protected]Aashna SinhaSchool of Applied and Life Sciences, Division of Research and Innovation, Uttaranchal University, Dehradun, Uttarakhand, India. Electronic address: [email protected]Sitora Amirovna TilyavovaDepartment of Obstetrics and Gynaecology, Samarkand State Medical University, Samarkand, Uzbekistan. Electronic address: [email protected]Hayder Naji SameerCollage of Pharmacy, National University of Science and Technology, Dhi Qar, 64001, Iraq. Electronic address: [email protected]Ahmed YaseenGilgamesh Ahliya University, Baghdad, Iraq. Electronic address: [email protected]Rasim Mahdi SalihDepartment of Pharmacy, Al-Zahrawi University College, Karbala, Iraq. Electronic address: [email protected]Mohaned AdilPharmacy college, Al-Farahidi University, Iraq. Electronic address: [email protected]

Cancer Treatment and Research Communicationsjournal2026en

ABI

Аннотация

MicroRNA-155 (miR-155) is a crucial miRNA that connects inflammation signaling with epigenetic regulation, impacting programmed cell death (PCD) and influencing chemotherapy resistance. It inhibits apoptosis by targeting pro-apoptotic factors and adjusts autophagy via PDK1/AKT-mTOR activation or downregulating ATG5, helping cells cope with stress. In many solid and hematologic cancers, the predominant pattern involves promoting resistance, mainly through miR-155-5p-driven suppression of pro-apoptotic or checkpoint regulators, involving PI3K/AKT, NF-κB, and STAT3 pathways. Conversely, some studies indicate chemosensitizing or tumor-suppressive roles in specific contexts, such as miR-155-3p/MYD88 signaling in breast cancer, miR-155/XIAP in ovarian cancer, and miR-155/CD47-TNFAIP8 in multiple myeloma. miR-155 also influences autophagy depending on the context, either promoting protective autophagy by targeting mTOR pathway regulators or enhancing chemosensitivity by suppressing key autophagy components like ATG5. New findings associate miR-155 with pyroptosis, necroptosis, and immune clearance via phagocytosis, though the mechanisms vary across pathways. In the tumor microenvironment, exosomal miR-155 spreads resistance traits, such as epithelial-mesenchymal transition, stemness, and survival signaling in adjacent cells. Therapeutic approaches include inhibition or restoration, tailored to isoform, tumor type, and network, with growing support for oligonucleotide-based therapies, nanoparticle delivery, and combination treatments. Overall, miR-155 is a powerful biomarker for chemoresistance and a promising therapeutic target, especially when strategies are isoform- and context-specific. This review adopts a mechanism-first approach to distinguish common resistance modules from true context-dependent exceptions, highlighting isoform specificity and translational relevance.

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Мавзулар

MicroRNA in disease regulation Phagocytosis and Immune Regulation Extracellular vesicles in disease

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DOI: 10.1016/j.ctarc.2026.101198

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