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B4GALNT1 enhances cell proliferation and growth in oral squamous cell carcinoma via p38 and JNK MAPK pathway
BACKGROUND: Beta-1,4-N-Acetyl-Galactosaminyltransferase 1 (B4GALNT1) was reported to play an important role in the development of the central nervous systems. We found higher expression of B4GALNT1 in oral squamous cell carcinoma (OSCC) tissues compared to the paired normal adjacent tissues in the T...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
AME Publishing Company
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8799079/ https://www.ncbi.nlm.nih.gov/pubmed/35117594 http://dx.doi.org/10.21037/tcr.2020.03.73 |
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author | Jing, Shaohong Deng, Zhaoming Liang, Lizhong Liang, Jun |
author_facet | Jing, Shaohong Deng, Zhaoming Liang, Lizhong Liang, Jun |
author_sort | Jing, Shaohong |
collection | PubMed |
description | BACKGROUND: Beta-1,4-N-Acetyl-Galactosaminyltransferase 1 (B4GALNT1) was reported to play an important role in the development of the central nervous systems. We found higher expression of B4GALNT1 in oral squamous cell carcinoma (OSCC) tissues compared to the paired normal adjacent tissues in the TCGA database. This study aimed to investigate whether there was a potential relationship between B4GALNT1 and OSCC tumorigenesis and further explored the possible regulation mechanism. METHODS: Gene expression level was analyzed by means of real-time quantitative PCR and further cell function experiments were performed including cell proliferation and apoptosis test, cell cycle distribution detection after silencing B4GALNT1 by transfection with B4GALNT1-shRNA lentivirus. Western Blotting was carried out to explore the possible molecular mechanism. RESULTS: The present study confirmed the overexpression of B4GALNT1 in OSCC. Compared to the control group, cell proliferation after silencing B4GALNT1 was significantly inhibited and cell apoptosis percentage was significantly higher. Besides, the knockdown of B4GALNT1 resulted in cell cycle arrest at G1 phase in our experiment. CONCLUSIONS: B4GALNT1 enhances the proliferation and suppress the apoptosis of OSCC cells probably through JNK and p38 signaling pathway. |
format | Online Article Text |
id | pubmed-8799079 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | AME Publishing Company |
record_format | MEDLINE/PubMed |
spelling | pubmed-87990792022-02-02 B4GALNT1 enhances cell proliferation and growth in oral squamous cell carcinoma via p38 and JNK MAPK pathway Jing, Shaohong Deng, Zhaoming Liang, Lizhong Liang, Jun Transl Cancer Res Original Article BACKGROUND: Beta-1,4-N-Acetyl-Galactosaminyltransferase 1 (B4GALNT1) was reported to play an important role in the development of the central nervous systems. We found higher expression of B4GALNT1 in oral squamous cell carcinoma (OSCC) tissues compared to the paired normal adjacent tissues in the TCGA database. This study aimed to investigate whether there was a potential relationship between B4GALNT1 and OSCC tumorigenesis and further explored the possible regulation mechanism. METHODS: Gene expression level was analyzed by means of real-time quantitative PCR and further cell function experiments were performed including cell proliferation and apoptosis test, cell cycle distribution detection after silencing B4GALNT1 by transfection with B4GALNT1-shRNA lentivirus. Western Blotting was carried out to explore the possible molecular mechanism. RESULTS: The present study confirmed the overexpression of B4GALNT1 in OSCC. Compared to the control group, cell proliferation after silencing B4GALNT1 was significantly inhibited and cell apoptosis percentage was significantly higher. Besides, the knockdown of B4GALNT1 resulted in cell cycle arrest at G1 phase in our experiment. CONCLUSIONS: B4GALNT1 enhances the proliferation and suppress the apoptosis of OSCC cells probably through JNK and p38 signaling pathway. AME Publishing Company 2020-04 /pmc/articles/PMC8799079/ /pubmed/35117594 http://dx.doi.org/10.21037/tcr.2020.03.73 Text en 2020 Translational Cancer Research. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/. |
spellingShingle | Original Article Jing, Shaohong Deng, Zhaoming Liang, Lizhong Liang, Jun B4GALNT1 enhances cell proliferation and growth in oral squamous cell carcinoma via p38 and JNK MAPK pathway |
title | B4GALNT1 enhances cell proliferation and growth in oral squamous cell carcinoma via p38 and JNK MAPK pathway |
title_full | B4GALNT1 enhances cell proliferation and growth in oral squamous cell carcinoma via p38 and JNK MAPK pathway |
title_fullStr | B4GALNT1 enhances cell proliferation and growth in oral squamous cell carcinoma via p38 and JNK MAPK pathway |
title_full_unstemmed | B4GALNT1 enhances cell proliferation and growth in oral squamous cell carcinoma via p38 and JNK MAPK pathway |
title_short | B4GALNT1 enhances cell proliferation and growth in oral squamous cell carcinoma via p38 and JNK MAPK pathway |
title_sort | b4galnt1 enhances cell proliferation and growth in oral squamous cell carcinoma via p38 and jnk mapk pathway |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8799079/ https://www.ncbi.nlm.nih.gov/pubmed/35117594 http://dx.doi.org/10.21037/tcr.2020.03.73 |
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