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miR-1207-5p suppresses laryngeal squamous cell carcinoma progression by downregulating SKA3 and inhibiting epithelial-mesenchymal transition.

Authors :
Wu Y
Dai F
Zhang Y
Zheng X
Li L
Zhang Y
Cao J
Gao W
Source :
Molecular therapy oncolytics [Mol Ther Oncolytics] 2021 Aug 19; Vol. 22, pp. 152-165. Date of Electronic Publication: 2021 Aug 19 (Print Publication: 2021).
Publication Year :
2021

Abstract

Laryngeal squamous cell carcinoma (LSCC) is the second most common head and neck cancer. Previously, we discovered that miR-1207-5p was downregulated in LSCC. In this study, the clinical significance, function, and mechanism of miR-1207-5p in LSCC were investigated. Downregulation of miR-1207-5p was found to be strongly linked to the malignant progression of LSCC. Functional studies revealed that miR-1207-5p upregulation suppressed LSCC cell proliferation, invasion, migration, and xenograft tumor growth. Bioinformatics analysis revealed that miR-1207-5p target genes were involved in cell cycle regulation, proliferation, adhesion, and the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Mechanistic studies revealed that miR-1207-5p interacts directly with the 3' untranslated region of spindle and kinetochore associated complex subunit 3 (SKA3) and downregulates SKA3 expression. Furthermore, SKA3 was found to be overexpressed in LSCC, and its high expression was associated with tumor progression and a poor prognosis. Rescue experiments demonstrated that miR-1207-5p inhibited the malignant phenotypes of LSCC via SKA3. Furthermore, miR-1207-5p upregulation or knockdown of SKA3 inhibited the epithelial-mesenchymal transition (EMT). Collectively, miR-1207-5p inhibited LSCC malignant progression by downregulating SKA3 and preventing EMT. These findings provide new insights into the mechanism of LSCC progression, as well as new potential biomarkers and therapeutic targets for LSCC diagnosis and treatment.<br />Competing Interests: The authors declare no competing interests.<br /> (© 2021 The Author(s).)

Details

Language :
English
ISSN :
2372-7705
Volume :
22
Database :
MEDLINE
Journal :
Molecular therapy oncolytics
Publication Type :
Academic Journal
Accession number :
34514096
Full Text :
https://doi.org/10.1016/j.omto.2021.08.001