ArticleExperimental and molecular pathology2010
Epigenetic modifications induced by RGC-32 in colon cancer.
Article in Experimental and molecular pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 47 citations in OpenAlex.
- New insights into the role of complement system in colorectal cancer (Review).Molecular medicine reports · 2025Review
- Uncovering immune cell heterogeneity in hepatocellular carcinoma by combining single-cell RNA sequencing with T-cell receptor sequencing.World journal of hepatology · 2025Article
- Response gene to complement 32 promotes tumorigenesis by mediating DNA damage repair and inhibits CD8+ T cells infiltration in diffuse large B-cell lymphoma.Frontiers in immunology · 2025Article
- Response Gene to Complement 32 promotes cell proliferation and tamoxifen resistance in breast cancer via elevated FoxM1 expression.PloS one · 2025Article
- Epigenetic Alteration in Colorectal Cancer: Potential Diagnostic and Prognostic Implications.International journal of molecular sciences · 2024Review
- Loss of feedback regulation between FAM3B and androgen receptor driving prostate cancer progression.Journal of the National Cancer Institute · 2024Article
- Bioactive glass selectively promotes cytotoxicity towards giant cell tumor of bone derived neoplastic stromal cells and induces MAPK signalling dependent autophagy.Bioactive materials · 2022Article
- RGCC balances self-renewal and neuronal differentiation of neural stem cells in the developing mammalian neocortex.EMBO reports · 2021Article
- Sublytic C5b-9 induces proliferation of glomerular mesangial cells via ERK5/MZF1/RGC-32 axis activated by FBXO28-TRAF6 complex.Journal of cellular and molecular medicine · 2019Article
- RGC-32 and diseases: the first 20 years.Immunologic research · 2019Review
- Role of C5b-9 and RGC-32 in Cancer.Frontiers in immunology · 2019Review
- Loss of Response Gene to Complement 32 (RGC-32) in Diabetic Mouse Retina Is Involved in Retinopathy Development.International journal of molecular sciences · 2018Article
- RGC-32 (Response Gene to Complement 32) Deficiency Protects Endothelial Cells From Inflammation and Attenuates Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Response Gene to Complement 32 in Vascular Diseases.Frontiers in cardiovascular medicine · 2018Review
- Renal proteomic analysis of RGC-32 knockout mice reveals the potential mechanism of RGC-32 in regulating cell cycle.American journal of translational research · 2018Article
- The complement system as a biomarker of disease activity and response to treatment in multiple sclerosis.Immunologic research · 2017Review
- RGC-32 Promotes Th17 Cell Differentiation and Enhances Experimental Autoimmune Encephalomyelitis.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- RGC32 induces epithelial-mesenchymal transition by activating the Smad/Sip1 signaling pathway in CRC.Scientific reports · 2017Article
- The Role of Stem Cell DNA Methylation in Colorectal Carcinogenesis.Stem cell reviews and reports · 2016Review
- [Relationship of cystatin C, fibrinogen, and 24-hour urinary protein with renal pathological grade in children with Henoch-Schönlein purpura nephritis].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2016Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
First described as a cell cycle activator, RGC-32 is both an activator and a substrate for CDC2. Deregulation of RGC-32 expression has been detected in a wide variety of human cancers. We have now shown that RGC-32 is expressed in precancerous states, and its expression is significantly higher in adenomas than in normal colon tissue. The expression of RGC-32 was higher in advanced stages of colon cancer than in precancerous states or the initial stages of colon cancer. In order to identify the genes that are regulated by RGC-32, we used gene array analysis to investigate the effect of RGC-32 knockdown on gene expression in the SW480 colon cancer cell line. Of the 230 genes that were differentially regulated after RGC-32 knockdown, a group of genes involved in chromatin assembly were the most significantly regulated in these cells: RGC-32 knockdown induced an increase in acetylation of histones H2B lysine 5 (H2BK5), H2BK15, H3K9, H3K18, and H4K8. RGC-32 silencing was also associated with decreased expression of SIRT1 and decreased trimethylation of histone H3K27 (H3K27me3). In addition, RGC-32 knockdown caused a significantly higher percentage of SW480 cells to enter S phase and subsequently G2/M. These data suggest that RGC-32 may contribute to the development of colon cancer by regulating chromatin assembly.
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