miRNA-20a: A Dual Regulator of Cell Migration and Apoptosis in Oral Squamous Cell Carcinoma:– An In Vitro Study

Introduction: Oral squamous cell carcinoma (OSCC) is one of the many cancer types where microRNAs (miRs) are often found to be overexpressed. STAT3, a significant component of human cancer, is now well recognized in recent research and is regarded as an attractive target for the creation of novel an...

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Main Authors: Priya Thomas, Sushmaa Chandralekha Selvakumar, K. Auxzilia Preethi, Abilasha Ramasubramanian, Pratibha Ramani, Durairaj Sekar
Format: Article
Language:English
Published: Wolters Kluwer Medknow Publications 2023-01-01
Series:Journal of Orofacial Sciences
Subjects:
Online Access:http://www.jofs.in/article.asp?issn=0975-8844;year=2023;volume=15;issue=2;spage=167;epage=174;aulast=Thomas
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author Priya Thomas
Sushmaa Chandralekha Selvakumar
K. Auxzilia Preethi
Abilasha Ramasubramanian
Pratibha Ramani
Durairaj Sekar
author_facet Priya Thomas
Sushmaa Chandralekha Selvakumar
K. Auxzilia Preethi
Abilasha Ramasubramanian
Pratibha Ramani
Durairaj Sekar
author_sort Priya Thomas
collection DOAJ
description Introduction: Oral squamous cell carcinoma (OSCC) is one of the many cancer types where microRNAs (miRs) are often found to be overexpressed. STAT3, a significant component of human cancer, is now well recognized in recent research and is regarded as an attractive target for the creation of novel anti-cancer medications. We assessed the expression, functions, and mechanisms of miR-20a-3p and STAT3 in the regulation of OSCC cell proliferation, migration, and apoptosis to highlight the significance of miRNA dysregulation in cancer etiology. Materials and Methods: miR-20a-3p’s function was examined by transfecting KB cells with the miR-20a-3p and STAT3 plasmids, followed by cell proliferation (CCK-8) assays, migration, and apoptosis. Furthermore, the impact of miR-20a-3p on the expression of its target gene was investigated using a quantitative real-time polymerase chain reaction. The expression of miR-20a-3p, STAT3, and IL-6 was investigated using a quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Results: The findings indicated that miR-20a-3p was downregulated ad STAT3 was upregulated in OSCC cells. Elevated STAT3 levels in OSCC cells were associated with enhanced tumor cell proliferation, migration, decreased apoptosis, and upregulated IL-6 expression. In OSCC cells, the overexpression of miR-20a-3p was accompanied by a reduction in the production of STAT3 and IL-6. Conclusion: In conclusion, our work showed that miR-20a-3p served as a tumor suppressor in OSCC by reducing the proliferation and migration of cancer cells by inhibiting STAT3 expression.
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spelling doaj.art-eeb72f1055d84b70a86c9a1e2382f7c12024-02-22T15:03:50ZengWolters Kluwer Medknow PublicationsJournal of Orofacial Sciences0975-88442023-01-0115216717410.4103/jofs.jofs_330_23miRNA-20a: A Dual Regulator of Cell Migration and Apoptosis in Oral Squamous Cell Carcinoma:– An In Vitro StudyPriya ThomasSushmaa Chandralekha SelvakumarK. Auxzilia PreethiAbilasha RamasubramanianPratibha RamaniDurairaj SekarIntroduction: Oral squamous cell carcinoma (OSCC) is one of the many cancer types where microRNAs (miRs) are often found to be overexpressed. STAT3, a significant component of human cancer, is now well recognized in recent research and is regarded as an attractive target for the creation of novel anti-cancer medications. We assessed the expression, functions, and mechanisms of miR-20a-3p and STAT3 in the regulation of OSCC cell proliferation, migration, and apoptosis to highlight the significance of miRNA dysregulation in cancer etiology. Materials and Methods: miR-20a-3p’s function was examined by transfecting KB cells with the miR-20a-3p and STAT3 plasmids, followed by cell proliferation (CCK-8) assays, migration, and apoptosis. Furthermore, the impact of miR-20a-3p on the expression of its target gene was investigated using a quantitative real-time polymerase chain reaction. The expression of miR-20a-3p, STAT3, and IL-6 was investigated using a quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Results: The findings indicated that miR-20a-3p was downregulated ad STAT3 was upregulated in OSCC cells. Elevated STAT3 levels in OSCC cells were associated with enhanced tumor cell proliferation, migration, decreased apoptosis, and upregulated IL-6 expression. In OSCC cells, the overexpression of miR-20a-3p was accompanied by a reduction in the production of STAT3 and IL-6. Conclusion: In conclusion, our work showed that miR-20a-3p served as a tumor suppressor in OSCC by reducing the proliferation and migration of cancer cells by inhibiting STAT3 expression.http://www.jofs.in/article.asp?issn=0975-8844;year=2023;volume=15;issue=2;spage=167;epage=174;aulast=Thomasmir-20amigrationoral squamous cell carcinomastat3
spellingShingle Priya Thomas
Sushmaa Chandralekha Selvakumar
K. Auxzilia Preethi
Abilasha Ramasubramanian
Pratibha Ramani
Durairaj Sekar
miRNA-20a: A Dual Regulator of Cell Migration and Apoptosis in Oral Squamous Cell Carcinoma:– An In Vitro Study
Journal of Orofacial Sciences
mir-20a
migration
oral squamous cell carcinoma
stat3
title miRNA-20a: A Dual Regulator of Cell Migration and Apoptosis in Oral Squamous Cell Carcinoma:– An In Vitro Study
title_full miRNA-20a: A Dual Regulator of Cell Migration and Apoptosis in Oral Squamous Cell Carcinoma:– An In Vitro Study
title_fullStr miRNA-20a: A Dual Regulator of Cell Migration and Apoptosis in Oral Squamous Cell Carcinoma:– An In Vitro Study
title_full_unstemmed miRNA-20a: A Dual Regulator of Cell Migration and Apoptosis in Oral Squamous Cell Carcinoma:– An In Vitro Study
title_short miRNA-20a: A Dual Regulator of Cell Migration and Apoptosis in Oral Squamous Cell Carcinoma:– An In Vitro Study
title_sort mirna 20a a dual regulator of cell migration and apoptosis in oral squamous cell carcinoma an in vitro study
topic mir-20a
migration
oral squamous cell carcinoma
stat3
url http://www.jofs.in/article.asp?issn=0975-8844;year=2023;volume=15;issue=2;spage=167;epage=174;aulast=Thomas
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