ArticleBioengineered2022
Long non-coding RNA FAM83A antisense RNA 1 (lncRNA FAM83A-AS1) targets microRNA-141-3p to regulate lung adenocarcinoma cell proliferation, migration, invasion, and epithelial-mesenchymal transition progression.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Construction of PANoptosis-related lncRNA prognostic model and immunotherapy sensitivity analysis in lung adenocarcinoma.Journal of cardiothoracic surgery · 2026Article
- miR-141-3p inhibited BPA-induced proliferation and migration of lung cancer cells through PTGER4.Cytotechnology · 2025Article
- FAM83A-AS1 predicts severe development of non-small cell lung cancer and adverse postoperative prognosis of thoracotomy.Journal of cardiothoracic surgery · 2025Article
- Study on the Mechanism of Competing Endogenous Network of 'Current computer-aided drug design · 2025Article
- Integrated analysis reveals critical cisplatin-resistance regulators E2F7 contributed to tumor progression and metastasis in lung adenocarcinoma.Cancer cell international · 2024Article
- Construction of an EMT-related lncRNA prognostic signature for lung adenocarcinoma and functional verification of its hub gene LINC01615.Journal of cancer research and clinical oncology · 2023Article
- Interactions between circRNAs and miR-141 in Cancer: From Pathogenesis to Diagnosis and Therapy.International journal of molecular sciences · 2023Review
- High‑risk pathological subtype associated FAM83A‑AS1 promotes malignancy and glycolysis of lung adenocarcinoma via miR‑202‑3p/HK2 axis.Oncology reports · 2023Article
- LncRNA PCAT6 promotes proliferation, migration, invasion, and epithelial-mesenchymal transition of lung adenocarcinoma cell by targeting miR-545-3p.Molecular biology reports · 2023Article
- Cuproptosis-related LncRNAs signature as biomarker of prognosis and immune infiltration in pancreatic cancer.Frontiers in genetics · 2023Article
- Long non-coding RNA LINC01270 is an onco-promotor in lung adenocarcinoma by upregulating LARP1 via sponging miR-326.Bioengineered · 2022Article
- LINC00514 facilitates cell proliferation, migration, invasion, and epithelial-mesenchymal transition in non-small cell lung cancer by acting on the Wnt/β-catenin signaling pathway.Bioengineered · 2022Article
- FAM83A antisense RNA 1 (Bioengineered · 2022Article
- Cross-talk between necroptosis-related lncRNAs to construct a novel signature and predict the immune landscape of lung adenocarcinoma patients.Frontiers in genetics · 2022Article
- Identification of a apoptosis-related LncRNA signature to improve prognosis prediction and immunotherapy response in lung adenocarcinoma patients.Frontiers in genetics · 2022Article
- Necroptosis-related lncRNA in lung adenocarcinoma: A comprehensive analysis based on a prognosis model and a competing endogenous RNA network.Frontiers in genetics · 2022Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The current paper investigates how long non-coding RNA (lncRNA) FAM83A antisense RNA 1 (lncRNA FAM83A-AS1) affected the epithelial-mesenchymal transformation (EMT), growth, invasion and migration of lung adenocarcinoma (LUAD) via targeting miRNA-141-3p. The GEPIA and ENCORI databases were used to analyze differences in lncRNA FAM83A-AS1 levels within LUAD samples. FAM83A-AS1 and miR-141-3p levels were assessed using qRT-PCR among 30 LUAD samples and surrounding normal tissues. In addition, we analyzed how FAM83A-AS1 affected proliferation, invasion, migration, and EMT processes of LUAD cells by targeting miR-141-3p through EdU, CCK-8 assay, scratch assay, transwell migration and invasion assay, immunofluorescence (IF) staining and WB assay. MicroRNAs targeting FAM83A-AS1 were screened using AnnoLnc2 and identified by RT-qPCR. Dual-luciferase assays were utilized to evaluate the connection between FAM83A-AS1 and miR-141-3p. FAM83A-AS1 expression was remarkably raised in lung cancer cells and tissue samples; however, miR-141-3p level markedly reduced relative to healthy samples. FAM83A-AS1 silencing suppressed EMT, growth, invasion and migration of LUAD cells. MiR-141-3p was the possible FAM83A-AS1 binding target negatively associated with FAM83A-AS1. The miR-141-3p inhibitor partly abolished the FAM83A-AS1 knockdown-induced inhibition on EMT, cell growth, invasion and migration in LUAD cells. In addition, miR-141-3p down-regulation abolished the inhibition of E-box-bound zinc finger protein 1 and 2 protein production following FAM83A-AS1 knockdown. According to our results, FAM83A-AS1/miR-141-3p axis plays an important role in LUAD occurrence and development. FAM83A-AS1 sponged miR-141-3p to down-regulate the level of the latter within LUAD and thereby encouraging LUAD development and suggesting a possible novel therapeutic approach for LUAD.
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