ArticleExperimental and therapeutic medicine2020
Response gene to complement-32 promotes cell survival via the NF-κB pathway in non-small-cell lung cancer.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Article
- Metformin Inhibits the Progression of Pancreatic Cancer Through Regulating miR-378a-3p/VEGFA/RGC-32 Axis.Cancer medicine · 2024Article
- Nonylphenol Promoted Epithelial-Mesenchymal Transition in Colorectal Cancer Cells by Upregulating the Expression of Regulator of Cell Cycle.Chemical research in toxicology · 2022Article
- PINCH1 knockout aggravates myocardial infarction in mice via mediating the NF-κB signaling pathway.Experimental and therapeutic medicine · 2022Article
- Targeting the Complement Pathway in Malignant Glioma Microenvironments.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Response gene to complement (RGC)-32 regulates the cell cycle in response to complement activation. The present study demonstrated that the expression level of RGC-32 is higher in human non-small-cell lung cancer (NSCLC) tissues compared with health controls. Overexpressing RGC-32 induced p65 nucleus translocation, significantly increased nuclear p65 levels and promoted the proliferation of A549 cells. Knockdown of RGC-32 by short hairpin RNA decreased the expression level of nuclear p65 and inhibited cell proliferation. The increase in cell proliferation induced by RGC32 could be abolished by the NF-κB inhibitor pyrrolidine dithiocarbamate. Mechanistic studies indicated that RGC32 mediated NF-κB downstream genes, including vascular cell adhesion protein 1, interleukin-6, cyclin dependent kinase inhibitor 2C, testin and vascular endothelial growth factor A. In summary, the present study demonstrated a novel role of RGC-32 in the progression of NSCLC via the NF-κB pathway and p65. Therefore, RGC-32 could be a potential therapeutic target for NSCLC.
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Registered trials
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