ArticleCellular oncology (Dordrecht, Netherlands)2022
ITGA2 induces STING expression in pancreatic cancer by inducing DNMT1 degradation.
Article in Cellular oncology (Dordrecht, Netherlands), 2022. 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.
- DNMT1-Induced Downregulation of CBX7 Inhibits ERK Phosphorylation and Promotes Pancreatic Ductal Adenocarcinoma Progression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Machine learning model reveals the risk, prognosis, and drug response of histamine-related signatures in pancreatic cancer.Discover oncology · 2025Article
- Transcriptomic analysis reveals transcription factors implicated in radon-induced lung carcinogenesis.Toxicology research · 2024Article
- Integrin α2 in the microenvironment and the tumor compartment of digestive (gastrointestinal) cancers: emerging regulators and therapeutic opportunities.Frontiers in oncology · 2024Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
purposeIntegrin alpha 2 (ITGA2, also known as CD49b or VLA-2) is the alpha subunit of a transmembrane receptor for collagens and related proteins. Previously, we found that ITGA2 may regulate immune cell infiltration in pancreatic cancer by inducing PD-L1 expression. As yet, however, whether ITGA2 regulates immune cell infiltration in pancreatic cancer by other mechanisms remains unclear.
methodsRNA sequencing was performed to identify differentially expressed genes in ITGA2-silenced pancreatic cancer cells. Protein-protein interactions were detected via co-immunoprecipitation. The infiltration level of immune cells was assessed using an immunofluorescence staining assay.
resultsWe found that ITGA2 can activate the cytosolic DNA-sensing pathway and promote STING expression in pancreatic cancer cells. In addition, we found that ITGA2 induces DNMT1 degradation by disrupting the interaction between DNMT1 and Kindlin2 in pancreatic cancer cells. As a DNA methyltransferase, we found that DNMT1 overexpression induced by ITGA2 silencing significantly up-regulated the methylation level of the STING gene promoter. Finally, ITGA2 silencing combined with DNMT1 inhibitor treatment induced immune cell infiltration in pancreatic cancer.
conclusionOur data indicate that ITGA2 induces STING expression by interacting with DNMT1 and inducing the degradation of DNMT1. ITGA2 silencing combined with DNMT1 inhibitor treatment may be a novel therapeutic strategy for pancreatic cancer.
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