ArticleOncology letters2023
ABCA3, a tumor suppressor gene, inhibits the proliferation, migration and invasion of lung adenocarcinoma by regulating the epithelial‑mesenchymal transition process.
Article in Oncology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- CRISPR and compound screens in a novel ex vivo tissue model identify DDR1 and ETA as regulators of cancer cell invasion.Cellular & molecular biology letters · 2026Article
- Targeting ABCA3 impedes tumor progression and EGFR-TKI resistance in EGFR-mutant LUAD.Cancer cell international · 2026Article
- High-throughput methylation sequencing reveals novel biomarkers for the early detection of renal cell carcinoma.BMC cancer · 2025Article
- Single-cell dissection reveals immunosuppressive F13A1+ macrophage as a hallmark for multiple primary lung cancers.Clinical and translational medicine · 2024Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung adenocarcinoma (LUAD) is one of the most common types of lung cancer, which affects the life and health of patients. The role of ATP-binding cassette subfamily A member 3 (ABCA3) in the occurrence and development of LUAD is unclear; therefore, ABCA3 expression in LUAD and other tumors was analyzed in the present study. In addition, ABCA3 expression in patients with LUAD and their survival were analyzed using a public database. ABCA3 co-expressed genes were identified and their enriched pathways were analyzed. Furthermore, ABCA3 expression was knocked down in LUAD cell lines. The proliferation, invasion and migration of cells, and the process of epithelial-mesenchymal transition (EMT), were studied through cytological and molecular biology experiments. Compared with that in normal lung tissues, ABCA3 expression was significantly reduced in tumor tissues. Patients with low ABCA3 expression had a markedly worse overall survival compared with those with high ABCA3 expression. Notably, abnormal ABCA3 expression has been observed in a variety of tumors. Subsequently, multiple pathophysiological pathways enriched by ABCA3 and its co-expressed genes were explored. Furthermore, the malignant behavior of tumor cells was enhanced when ABCA3 expression was knocked down, and the EMT process was activated after ABCA3 expression was knocked down. In conclusion, as a tumor suppressor gene, ABCA3 serves a protective role in the development of tumors, and may have a potential role in clinical applications, and thus, is worthy of further study.
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