Intricate relationship between cancer stemness, metastasis, and drug resistance.

Autor: Dakal TC; Genome and Computational Biology Lab Department of Biotechnology Mohanlal Sukhadia University Udaipur Rajasthan India., Bhushan R; Department of Zoology M.S. College Motihari Bihar India., Xu C; Department of General Surgery The First Affiliated Hospital of Dalian Medical University Dalian China.; Department of Molecular Diagnostics and Experimental Therapeutics, Beckman Research Institute City of Hope Monrovia California USA., Gadi BR; Stress Physiology and Molecular Biology Laboratory Department of Botany Jai Narain Vyas University Jodhpur Rajasthan India., Cameotra SS; SAS Polyclinic Mohali Punjab India., Yadav V; School of Life Sciences Jawaharlal Nehru University New Delhi India., Maciaczyk J; Department of Stereotactic and Functional Neurosurgery University Hospital of Bonn Bonn Germany., Schmidt-Wolf IGH; Center for Integrated Oncology (CIO) Department of Integrated Oncology University Hospital Bonn Bonn Germany., Kumar A; Manipal Academy of Higher Education Manipal Karnataka India.; Institute of Bioinformatics International Technology Park Bangalore India., Sharma A; Department of Stereotactic and Functional Neurosurgery University Hospital of Bonn Bonn Germany.; Center for Integrated Oncology (CIO) Department of Integrated Oncology University Hospital Bonn Bonn Germany.
Jazyk: angličtina
Zdroj: MedComm [MedComm (2020)] 2024 Sep 21; Vol. 5 (10), pp. e710. Date of Electronic Publication: 2024 Sep 21 (Print Publication: 2024).
DOI: 10.1002/mco2.710
Abstrakt: Cancer stem cells (CSCs) are widely acknowledged as the drivers of tumor initiation, epithelial-mesenchymal transition (EMT) progression, and metastasis. Originating from both hematologic and solid malignancies, CSCs exhibit quiescence, pluripotency, and self-renewal akin to normal stem cells, thus orchestrating tumor heterogeneity and growth. Through a dynamic interplay with the tumor microenvironment (TME) and intricate signaling cascades, CSCs undergo transitions from differentiated cancer cells, culminating in therapy resistance and disease recurrence. This review undertakes an in-depth analysis of the multifaceted mechanisms underlying cancer stemness and CSC-mediated resistance to therapy. Intrinsic factors encompassing the TME, hypoxic conditions, and oxidative stress, alongside extrinsic processes such as drug efflux mechanisms, collectively contribute to therapeutic resistance. An exploration into key signaling pathways, including JAK/STAT, WNT, NOTCH, and HEDGEHOG, sheds light on their pivotal roles in sustaining CSCs phenotypes. Insights gleaned from preclinical and clinical studies hold promise in refining drug discovery efforts and optimizing therapeutic interventions, especially chimeric antigen receptor (CAR)-T cell therapy, cytokine-induced killer (CIK) cell therapy, natural killer (NK) cell-mediated CSC-targeting and others. Ultimately use of cell sorting and single cell sequencing approaches for elucidating the fundamental characteristics and resistance mechanisms inherent in CSCs will enhance our comprehension of CSC and intratumor heterogeneity, which ultimately would inform about tailored and personalized interventions.
Competing Interests: All authors have showed no conflict of interest.
(© 2024 The Author(s). MedComm published by Sichuan International Medical Exchange & Promotion Association (SCIMEA) and John Wiley & Sons Australia, Ltd.)
Databáze: MEDLINE
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