MiR-154 inhibits the growth of laryngeal squamous cell carcinoma by targeting GALNT7.

Abstract

MicroRNAs are critical regulators of the development and progression of laryngeal squamous cell carcinoma (LSCC). However, the role of microRNA-154 (miR-154) in the development and progression of LSCC has not been clarified. We found that down-regulated miR-154 expression in LSCC tissues was associated with poorer prognosis in LSCC patients. MiR-154 over-expression inhibited the proliferation, clonogenicity, and migration of LSCC cells and induced cell cycle arrest, which were reversed by miR-154 inhibition. MiR-154 targeted GALNT7 expression by reducing GALNT7-regulated luciferase activity in LSCC cells while up-regulating GALNT7 mRNA transcription in LSCC tissues and cells. GALNT7 silencing significantly attenuated the proliferation, clonogenicity, and migration of LSCC cells and induced cell cycle arrest. Finally, intravenous treatment with lentivirus for miR-154, but not scrambled control miRNA, significantly restrained the growth of implanted LSCC Hep-2 tumors and decreased the tumor mass by reducing GALNT7 expression in mice. Therefore, miR-154 may serve as a novel prognostic marker and therapeutic target for LSCC.

• Authors: Jun-Tao Niu, Li-Jun Zhang, Yong-Wang Huang, Chao Li, Ning Jiang, Yuan-Jie Niu
• Journal: Biochemistry and cell biology = Biochimie et biologie cellulaire (Biochem Cell Biol) Vol. 96 Issue 6 Pg. 752-760 (12 2018) ISSN: 1208-6002 [Electronic] Canada
• PMID: 29874469 (Publication Type: Journal Article, Retracted Publication)

Chemical References

• Biomarkers, Tumor
• MIRN154 microRNA, human
• MicroRNAs
• RNA, Messenger
• N-Acetylgalactosaminyltransferases

Topics

• Biomarkers, Tumor (genetics, metabolism)
• Carcinoma, Squamous Cell (genetics, metabolism, pathology)
• Cell Cycle Checkpoints
• Cell Movement
• Cell Proliferation
• Cells, Cultured
• Female
• Humans
• Laryngeal Neoplasms (genetics, metabolism, pathology)
• Male
• MicroRNAs (genetics, metabolism)
• Middle Aged
• N-Acetylgalactosaminyltransferases (deficiency, genetics, metabolism)
• RNA, Messenger (antagonists & inhibitors, genetics, metabolism)
• Polypeptide N-acetylgalactosaminyltransferase