ArticleOncology reports2024
Identification of ITGB4 as a novel tumor promoting gene in lung adenocarcinoma (LUAD).
Article in Oncology reports, 2024. 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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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Potential Benefits of Metformin Via Roseburia Intestinalis in High-fat Diet-fed Mice With Colorectal Adenomas.Probiotics and antimicrobial proteins · 2026Article
- Non-coding RNAs modulation in breast cancer radioresponse: mechanisms and therapeutic implications.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2025Review
- ITGB4 is a prognostic biomarker and correlated with lung adenocarcinoma brain metastasis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Article
- Pharmacological targeting of adaptor proteins in chronic inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As the most frequently diagnosed cancer, lung cancer (LC) is the most common cause of cancer‑related death worldwide. In total, ~85% of malignant lung tumors belong to non‑small cell LC, of which ~50% are lung adenocarcinoma (LUAD). Integrin subunit β4 (ITGB4) is upregulated in lung glandular cancer and elevated ITGB4 levels predict an adverse clinical outcome. However, the biological function of ITGB4 in promoting LUAD progression remains unclear. In the present study, the upregulation of ITGB4 in LUAD tissue samples was demonstrated. To understand the biological role of ITGB4, ITGB4 expression was knocked down in A549 and PC9 cells through transfection with specific small interfering RNAs. The results demonstrated that the downregulation of ITGB4 attenuated A549 and PC9 cell proliferation, promoted cell apoptosis and inhibited colony formation, cell migration and cell invasion. To understand the mechanism of ITGB4, high throughput sequencing was performed using ITGB4‑knocked down A549 cells, followed by bioinformatics analysis. It was found that the genes upregulated by ITGB4 were significantly enriched in metabolism and related pathways, and the genes downregulated by ITGB4 were enriched in cell cycle and related pathways. In conclusion, the findings of the present study highlighted the oncogenic function of ITGB4 in LUAD and uncovered potential mechanisms fundamental to the progression of the disease.
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