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Research Paper|Volume 13, Issue 2|pp 2379—2396

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

Zheqi Liu1,2, Wenkai Zhou1,2, Chengzhong Lin2,3, Xiaoning Wang1,2, Xu Zhang1,2, Yu Zhang1,2, Rong Yang1,2, Wantao Chen1,2, Wei Cao1,2
  • 1Department of Oral and Maxillofacial, Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011 China
  • 2Shanghai Key Laboratory of Stomatology, Shanghai Research Institute of Stomatology, National Clinical Research Center of Stomatology, Shanghai 200011, China
  • 3Second Dental Clinic, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China
* Co-first authors
Received: June 13, 2020Accepted: October 31, 2020Published: December 9, 2020
https://doi.org/10.18632/aging.202268

Copyright: © 2020 Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

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.