4.6 Article

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

Journal

AGING-US
Volume 13, Issue 2, Pages 2379-2396

Publisher

IMPACT JOURNALS LLC

Keywords

FOXD2-AS1; OSCC; prognostic model; proliferation; migration

Funding

  1. National Natural Science Foundation of China [81972589, 81672745, 81702675]
  2. Program of Innovative Research Team of High-level Local Universities in Shanghai

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FOXD2-AS1 is closely associated with clinical characteristics in oral squamous cell carcinoma, and its high expression predicts poor prognosis in patients. It functions by promoting cell proliferation and migration, suppressing adaptive immunity, and participating in the development of oral squamous cell carcinoma.
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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