ArticleOncology letters2022
Silencing of integrin subunit α3 inhibits the proliferation, invasion, migration and autophagy of esophageal squamous cell carcinoma cells.
Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Enhanced ITGA3 expression induced by helicobacter pylori infection facilitates gastric cancer progression via NF-κB and Smad4.Molecular and cellular biochemistry · 2026Article
- A novel anoikis resistance-associated gene model for prognostic prediction and immune microenvironment characterization in lung squamous cell carcinoma.Discover oncology · 2026Article
- HEYL-mediated activation of LAMA3 influences radiotherapy response in esophageal cancer.Esophagus : official journal of the Japan Esophageal Society · 2025Article
- Identification of Autophagy-Related Prognostic Signature for Glioblastoma Standard Therapy.Biomolecules & therapeutics · 2025Article
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- Bioinformatics analysis revealsTranslational cancer research · 2024Article
- A prognostic model for anoikis-related genes in pancreatic cancer.Scientific reports · 2024Article
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Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal squamous cell carcinoma (ESCC) is a deadly disease that seriously affects global public health. The aim of the present study was to explore the role of integrin subunit α3 (ITGA3) in ESCC and investigate its detailed molecular mechanisms. Using reverse transcription-quantitative PCR (RT-qPCR) and western blotting, the mRNA and protein expression of ITGA3 in cell lines was detected. In addition, a series of cellular biological experiments, including Cell Counting Kit-8, wound-healing, Transwell and TUNEL assays, were used to evaluate proliferation, migration, invasion and apoptosis, respectively. Furthermore, western blotting was used to measure the expression of corresponding proteins. ITGA3 was found to be upregulated in ESCC cell lines (ECA109 and TE1). It was also found that ITGA3 silencing inhibited the proliferation, migration, invasion and autophagy of ECA109 and TE1 cells but promoted their apoptosis. In addition, ITGA3 silencing was found to inhibit the FAK/PI3K/AKT signaling pathway. In conclusion, ITGA3 knockdown suppressed cell proliferation, invasion, migration and autophagy in ECA109 and TE1 cells, suggesting that ITGA3 may be a potential therapeutic target for the treatment of ESCC.
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Registered trials
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