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Dysregulation of FOXD2-AS1 promotes cell proliferation and migration and predicts poor prognosis in oral squamous cell carcinoma: a study based on TCGA data

FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) plays an important role in the pathogenesis of some cancers. However, its functional role in oral squamous cell carcinoma (OSCC) remains largely unknown. In this study, we conducted expressional and functional analyses of FOXD2-AS1 using data from the...

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Autores principales: Liu, Zheqi, Zhou, Wenkai, Lin, Chengzhong, Wang, Xiaoning, Zhang, Xu, Zhang, Yu, Yang, Rong, Chen, Wantao, Cao, Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7880351/
https://www.ncbi.nlm.nih.gov/pubmed/33318296
http://dx.doi.org/10.18632/aging.202268
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author Liu, Zheqi
Zhou, Wenkai
Lin, Chengzhong
Wang, Xiaoning
Zhang, Xu
Zhang, Yu
Yang, Rong
Chen, Wantao
Cao, Wei
author_facet Liu, Zheqi
Zhou, Wenkai
Lin, Chengzhong
Wang, Xiaoning
Zhang, Xu
Zhang, Yu
Yang, Rong
Chen, Wantao
Cao, Wei
author_sort Liu, Zheqi
collection PubMed
description FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) plays an important role in the pathogenesis of some cancers. However, its functional role in oral squamous cell carcinoma (OSCC) remains largely unknown. In this study, we conducted expressional and functional analyses of FOXD2-AS1 using data from the Cancer Genome Atlas (TCGA) and in vitro OSCC assays. FOXD2-AS1 dysregulation was remarkably associated with radiation therapy, anatomic location, high histologic grade, and lymphovascular invasion (P < 0.05). A nomogram based on FOXD2-AS1 expression was constructed for use as a diagnostic indicator for OSCC patients, and multivariate cox regression analysis showed that FOXD2-AS1 expression was an independent prognostic factor for OSCC patients. KEGG, gene set enrichment analysis, and immune infiltration evaluations indicated that FOXD2-AS1 was involved in tumor progression via epithelial-to-mesenchymal transition and cell cycle regulation and was negatively associated with mast cell, DCs, iDCs, and B cells. FOXD2-AS1 silencing suppressed the proliferation and migration of Cal27 cells. Our findings showed that an aberrantly high FOXD2-AS1 expression predicts poor prognosis in OSCC; FOXD2-AS1 may act as an oncogenic protein by regulating cell proliferation and migration and may suppress adaptive immunity by modulating the number and function of antigen-presenting cells.
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spelling pubmed-78803512021-02-22 Dysregulation of FOXD2-AS1 promotes cell proliferation and migration and predicts poor prognosis in oral squamous cell carcinoma: a study based on TCGA data Liu, Zheqi Zhou, Wenkai Lin, Chengzhong Wang, Xiaoning Zhang, Xu Zhang, Yu Yang, Rong Chen, Wantao Cao, Wei Aging (Albany NY) Research Paper FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) plays an important role in the pathogenesis of some cancers. However, its functional role in oral squamous cell carcinoma (OSCC) remains largely unknown. In this study, we conducted expressional and functional analyses of FOXD2-AS1 using data from the Cancer Genome Atlas (TCGA) and in vitro OSCC assays. FOXD2-AS1 dysregulation was remarkably associated with radiation therapy, anatomic location, high histologic grade, and lymphovascular invasion (P < 0.05). A nomogram based on FOXD2-AS1 expression was constructed for use as a diagnostic indicator for OSCC patients, and multivariate cox regression analysis showed that FOXD2-AS1 expression was an independent prognostic factor for OSCC patients. KEGG, gene set enrichment analysis, and immune infiltration evaluations indicated that FOXD2-AS1 was involved in tumor progression via epithelial-to-mesenchymal transition and cell cycle regulation and was negatively associated with mast cell, DCs, iDCs, and B cells. FOXD2-AS1 silencing suppressed the proliferation and migration of Cal27 cells. Our findings showed that an aberrantly high FOXD2-AS1 expression predicts poor prognosis in OSCC; FOXD2-AS1 may act as an oncogenic protein by regulating cell proliferation and migration and may suppress adaptive immunity by modulating the number and function of antigen-presenting cells. Impact Journals 2020-12-09 /pmc/articles/PMC7880351/ /pubmed/33318296 http://dx.doi.org/10.18632/aging.202268 Text en Copyright: © 2020 Liu et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Liu, Zheqi
Zhou, Wenkai
Lin, Chengzhong
Wang, Xiaoning
Zhang, Xu
Zhang, Yu
Yang, Rong
Chen, Wantao
Cao, Wei
Dysregulation of FOXD2-AS1 promotes cell proliferation and migration and predicts poor prognosis in oral squamous cell carcinoma: a study based on TCGA data
title Dysregulation of FOXD2-AS1 promotes cell proliferation and migration and predicts poor prognosis in oral squamous cell carcinoma: a study based on TCGA data
title_full Dysregulation of FOXD2-AS1 promotes cell proliferation and migration and predicts poor prognosis in oral squamous cell carcinoma: a study based on TCGA data
title_fullStr Dysregulation of FOXD2-AS1 promotes cell proliferation and migration and predicts poor prognosis in oral squamous cell carcinoma: a study based on TCGA data
title_full_unstemmed Dysregulation of FOXD2-AS1 promotes cell proliferation and migration and predicts poor prognosis in oral squamous cell carcinoma: a study based on TCGA data
title_short Dysregulation of FOXD2-AS1 promotes cell proliferation and migration and predicts poor prognosis in oral squamous cell carcinoma: a study based on TCGA data
title_sort dysregulation of foxd2-as1 promotes cell proliferation and migration and predicts poor prognosis in oral squamous cell carcinoma: a study based on tcga data
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7880351/
https://www.ncbi.nlm.nih.gov/pubmed/33318296
http://dx.doi.org/10.18632/aging.202268
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