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The microRNA-6510 as a potential tumor suppressor in head and neck cancer.

作者信息

Sobecka-Giel Agnieszka, Ostrowska Kamila, Golusinski Wojciech, Suchorska Wiktoria M, Masternak Michal M, Golusinski Pawel

机构信息

Department of Head and Neck Surgery, Poznan University of Medical Sciences, Poznan, 61-701, Poland.

Radiobiology Lab, Department of Medical Physics, Greater Poland Cancer Centre, Poznan, 61-866, Poland.

出版信息

Sci Rep. 2025 Feb 18;15(1):5830. doi: 10.1038/s41598-025-86796-0.

Abstract

Head and Neck Squamous Cell Carcinoma (HNSCC) is the sixth most common cancer worldwide, with approximately 830,000 new cases and 430,000 deaths reported annually. Due to their heterogeneity, these neoplasms differ in their clinical course and response to the therapy. Therefore, it has become imperative to identify specific biological molecules that can potentially establish novel prognostic markers or targets for molecular therapy of HNSCC. MicroRNAs are a class of short, non-coding RNAs that function as post-transcriptional regulators of genes expression. They have been shown to be directly involved in oncogenesis, acting as tumor suppressors or oncogenes. Our previous study demonstrated that miRNA hsa-miR-6510-3p is significantly downregulated in tumor tissue compared to histologically normal tissue from HNSCC patients. Its significant downregulation in tumor tissue is associated with lower chances for recovery and patient's survival. This study aimed to determine the biological role of miR-6510-3p in HNSCC pathogenesis and its impact on biological processes occurring in cancer cells such as cell cycle, cell proliferation, migration or induction of cell death. We have also examined the impact of the miR-6510-3p on expression of cancer stem cell phenotype markers as well as on sensitivity of HNSCC cells to ionizing radiation. We observed that transfection of HNSCC cells with hsa-miR-6510-3p causes the cell cycle arrest in G2/M phase and is associated with a decrease of cell proliferation, migration and colony-forming ability of cancer cells. We have also demonstrated that hsa-miR-6510-3p induces cell death, increases the sensitivity of HNSCC cells to ionizing radiation and causes a loss of the stemness properties responsible for the occurrence of metastases and relapses of the disease. These results indicated the importance of miR-6510-3p as a marker and a driver of HNSCC disease.

摘要

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