ArticleOncology letters2021
FAM83A and FAM83A-AS1 both play oncogenic roles in lung adenocarcinoma.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Construction of PANoptosis-related lncRNA prognostic model and immunotherapy sensitivity analysis in lung adenocarcinoma.Journal of cardiothoracic surgery · 2026Article
- CLIC6 and ANLN: novel exosome-related prognostic markers and therapeutic targets in lung adenocarcinoma.Frontiers in immunology · 2026Article
- mMolecular cancer · 2023Article
- MiR-485-5p Suppress the Malignant Characteristics of the Lung Adenocarcinoma via Targeting NADPH Quinone Oxidoreductase-1 to Inhibit the PI3K/Akt.Molecular biotechnology · 2023Article
- Identification of natural killer cell associated subtyping and gene signature to predict prognosis and drug sensitivity of lung adenocarcinoma.Frontiers in genetics · 2023Article
- Construction and experimental validation of a necroptosis-related lncRNA signature as a prognostic model and immune-landscape predictor for lung adenocarcinoma.American journal of cancer research · 2023Article
- FAM83A antisense RNA 1 (Bioengineered · 2022Article
- Establishment of lung adenocarcinoma classification and risk model based on necroptosis-related genes.Frontiers in genetics · 2022Article
- LncRNA FAM83A-AS1 facilitates tumor proliferation and the migration via the HIF-1α/ glycolysis axis in lung adenocarcinoma.International journal of biological sciences · 2022Article
- YTHDF2 Inhibits the Migration and Invasion of Lung Adenocarcinoma by Negatively Regulating the FAM83D-TGFβ1-SMAD2/3 Pathway.Frontiers in oncology · 2022Article
- Choline Kinase: An Unexpected Journey for a Precision Medicine Strategy in Human Diseases.Pharmaceutics · 2021Review
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer. Nevertheless, the detailed molecular mechanisms of the progression of LUAD remain largely unknown. The present bioinformatics analysis reported that FAM83A and FAM83A-AS1 were upregulated in LUAD tissues and associated with prognosis in patients with LUAD. The purpose of the current study was to investigate the role of FAM83A and its antisense long non-coding (lnc)RNA FAM83A-AS1 in LUAD. Gene Expression Profiling Interactive Analysis was used to screen for potential oncogenes in LUAD and to analyze the clinical significance of FAM83A and FAM83A-AS1. Small interfering RNAs were constructed and transfected into LUAD cells to knock down the expression of FAM83A and FAM83A-AS1. EdU, Cell Counting Kit-8, Transwell and Matrigel assays were performed to detect the proliferation, migration and invasion of LUAD cells. The interaction between FAM83A-AS1, microRNA (miR)-495-3p and FAM83A was explored using a luciferase reporter assay. FAM83A and FAM83A-AS1 were both overexpressed in LUAD tissues compared with adjacent normal tissues. High expression of FAM83A and FAM83A-AS1 predicted worse survival and more advanced clinical stage. Knockdown of FAM83A or FAM83A-AS1 could inhibit the proliferation, migration and invasion of LUAD cells. Moreover, lncRNA FAM83A-AS1 regulated the expression of FAM83A by functioning as competing endogenous RNA for miR-495-3p. These results implicated that FAM83A and FAM83A-AS1 both played oncogenic roles in LUAD and FAM83A-AS1 could regulate the expression of FAM83A by sponging miR-495-3p. The study revealed a novel regulatory mechanism of tumor development in LUAD and FAM83A and FAM83A-AS1 may be novel biomarkers and therapeutic targets for LUAD.
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