MicroRNA325: A comprehensive exploration of its multifaceted roles in cancer pathogenesis and therapeutic implications (Review).
Oncol Lett
; 28(4): 459, 2024 Oct.
Article
in En
| MEDLINE
| ID: mdl-39119235
ABSTRACT
MicroRNA (miRNA/miR) represents a category of endogenous, short-chain non-coding RNA molecules comprising ~22 nucleotides. Specifically, miR-325 is situated within the first sub-band of region 2 on the short arm of the X chromosome. Notably, aberrant expression of miR-325 has been observed across various tumor systems, spanning the nervous, endocrine, respiratory, reproductive and digestive systems. miR-325 exhibits the capacity to target a minimum of 20 protein-coding genes, thereby influencing diverse cellular processes, including cell proliferation, epithelial-mesenchymal transition, apoptosis, invasion and migration. Moreover, miR-325 serves a pivotal role in the formation of six competing endogenous RNA (ceRNA) regulatory axes, involving one circular RNA, four long non-coding RNA and one additional miRNA. By participating in various signaling pathways through gene targeting, the abnormal expression of miR-325 has been associated with clinicopathological conditions in diverse patients with cancer, significantly impacting both the clinicopathology and prognosis of affected individuals. Additionally, miR-325 has been associated with the development of resistance to oxaliplatin, cisplatin and doxorubicin in cancer cells. Its involvement in the anticancer molecular mechanisms of these agents underscores its potential significance in therapeutic contexts. However, it is noteworthy that the current study did not specifically address sex-based cell line selection. In conclusion, the present review provides a comprehensive summary of the relevant findings concerning miR-325, offering valuable insights for future research endeavors focused on determining the molecular mechanisms associated with this miRNA.
Full text:
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Collection:
01-internacional
Database:
MEDLINE
Language:
En
Journal:
Oncol Lett
Year:
2024
Document type:
Article