Abstract

Human laryngeal squamous cell carcinoma (LSCC) is a malignant cancer type. Epithelial-mesenchymal transition marker Snail family transcriptional repressor 1 (SNAI1) is associated with the occurrence, development, invasion and metastasis of numerous tumor types, such as lung, liver and ovarian cancer. Previous studies have indicated that microRNA-153 (miR-153) may serve as a novel tumor suppressor, which is involved in tumor metastasis; however, the role and clinical significance of miR-153 in LSCC are not fully understood. The aim of the present study was to determine the role of miR-153 in the growth and aggressiveness of LSCC cells. Bioinformatics prediction method, western blot analysis, Matrigel invasion assay and immunofluorescence were used to analyze whether SNAI1 can be regulated and controlled by miR-153 in LSCC cells. An inverse association between miR-153 and SNAI1 was observed in LSCC tissues. It was demonstrated that SNAI1 is a direct target of miR-153 in LSCC. In addition, the results indicated that miR-153 knockdown inhibited PCI-13 cell migration and invasion by targeting SNAI1, which may be a potential marker that can reflect the degree of malignancy in patients with LSCC. Furthermore, miR-153 knockdown decreased Twist family BHLH transcription factor 1 and metastasis-associated 1 family member 3 expression in LSCC cells. In conclusion, these data indicated that miR-153 regulates LSCC migration via the targeting of SNAI1 gene, which may be a potential predictor for patients with LSCC.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.