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Competing Endogenous Rnas Regulatory Crosstalk Networks: The Messages From the Rna World to Signaling Pathways Directing Cancer Stem Cell Development Publisher



Aria H1, 2 ; Azizi M2 ; Nazem S3 ; Mansoori B4 ; Darbeheshti F5 ; Niazmand A6 ; Daraei A7, 8 ; Mansoori Y1, 9
Authors
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Authors Affiliations
  1. 1. Noncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran
  2. 2. Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
  3. 3. Department of Clinical Biochemistry, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Pediatrics Department, School of Medicine, Fasa University of Medical Sciences, Fasa, Iran
  5. 5. Department of Radiation Oncology, Dana-Farber Cancer Institute and Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States
  6. 6. Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
  7. 7. Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran
  8. 8. Department of Medical Genetics, School of Medicine, Babol University of Medical Sciences, Babol, Iran
  9. 9. Department of Medical Genetics, Fasa University of Medical Sciences, Fasa, Iran

Source: Heliyon Published:2024


Abstract

Cancer stem cells (CSCs) are one of the cell types that account for cancer heterogeneity. The cancer cells arrest in G0 and generate non-CSC progeny through self-renewal and pluripotency, resulting in tumor recurrence, metastasis, and resistance to chemotherapy. They can stimulate tumor relapse and re-grow a metastatic tumor. So, CSCs is a promising target for eradicating tumors, and developing an anti-CSCs therapy has been considered. In recent years competing endogenous RNA (ceRNA) has emerged as a significant class of post-transcriptional regulators that affect gene expression via competition for microRNA (miRNA) binding. Furthermore, aberrant ceRNA expression is associated with tumor progression. Recent findings show that ceRNA network can cause tumor progression through the effect on CSCs. To overcome therapeutic resistance due to CSCs, we need to improve our current understanding of the mechanisms by which ceRNAs are implicated in CSC-related relapse. Thus, this review was designed to discuss the role of ceRNAs in CSCs' function. Targeting ceRNAs may open the path for new cancer therapeutic targets and can be used in clinical research. © 2024 The Authors
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