Competing endogenous RNAs regulatory crosstalk networks: The messages from the RNA world to signaling pathways directing cancer stem cell development

(2024) Competing endogenous RNAs regulatory crosstalk networks: The messages from the RNA world to signaling pathways directing cancer stem cell development. Heliyon. p. 28.

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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.

Item Type: Article
Keywords: Cancer stem cells Competing endogenous RNAs ceRNA lncRNA Micro-RNA long noncoding rna epithelial-mesenchymal transition predicts poor-prognosis factor 4 klf4 prostate-cancer tumor-suppressor gastric-cancer bladder-cancer colon-cancer self-renewal Science & Technology - Other Topics
Page Range: p. 28
Journal or Publication Title: Heliyon
Journal Index: ISI
Volume: 10
Number: 15
Identification Number: https://doi.org/10.1016/j.heliyon.2024.e35208
Depositing User: خانم ناهید ضیائی
URI: http://eprints.mui.ac.ir/id/eprint/29966

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