Abstract

Oral squamous cell carcinoma (OSCC) has become the most common HPV-related cancer with high invasion and metastasis. Exploring biomarkers for the screening and monitoring of OSCC, especially for the HPV-OSCC, would benefit patients' diagnosis and prognosis. This study evaluated the significance and mechanism of TMEM161B-AS1 and miR-651-5p in HPV-OSCC aiming to provide novel insight into the mechanism of HPV-OSCC development. Expression of TMEM161B-AS1 and miR-561-5p was analyzed in healthy individuals, HPV-infected non-OSCC patients, and HPV-OSCC patients using PCR. Their significance in HPV-OSCC occurrence and prognosis was evaluated by logistic regression, ROC, Kaplan-Meier, and Cox regression analysis. In OSCC cells, CCK8 and Transwell assays were employed for assessing cell growth and metastasis. The luciferase reporter assay and cell transfection were performed to evaluate the regulatory association between TMEM161B-AS1, miR-561-5p, and BDNF. Significant upregulation of TMEM161B-AS1 and downregulation of miR-561-5p were observed in oral HPV-infected patients. Both TMEM161B-AS1 and miR-651-5p served as risk factors for the occurrence of OSCC in oral HPV-infected patients and could distinguish HPV-OSCC patients from HPV-infected non-OSCC patients. Increased TMEM161B-AS1 and reduced miR-561-5p indicated severe development and adverse prognosis of HPV-OSCC patients. In OSCC cells, silencing TMEM161-AS1 suppressed cell proliferation and motility via negatively modulating miR-561-5p. miR-561-5p negatively regulated BDNF, which was considered the underlying mechanism of TMEM161B-AS1. Increasing TMEM161B-AS expression and decreasing miR-561-5p showed the occurrence of OSCC in HPV-infected patients and predicted malignant development and adverse prognosis. TMEME161B-AS1 served as a tumor promoter via regulating the miR-561-5p/BDNF axis.

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.