ArticleThe Journal of biological chemistry2010
Induction of the apoptosis inhibitor ARC by Ras in human cancers.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The trial behind it
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
23 citing papers in PubMed, 33 citations in OpenAlex.
- Local control of Cre-regulated genetic modeling in vivo using wireless implantable optoelectronics.Science advances · 2026Article
- Comparative analysis of metabolome and transcriptomes to explore the inhibited influence of sonodynamic therapy combined with lonidamine on hepatocellular carcinoma.Drug delivery · 2025Article
- Role of apoptosis repressor with caspase recruitment domain in human health and chronic diseases.Annals of medicine · 2024Review
- A double-edged sword: role of apoptosis repressor with caspase recruitment domain (ARC) in tumorigenesis and ischaemia/reperfusion (I/R) injury.Apoptosis : an international journal on programmed cell death · 2023Review
- Expression of apoptosis repressor with caspase recruitment domain (ARC) in familial adenomatous polyposis (FAP) adenomas and its correlation with DNA mismatch repair proteins, p53, Bcl-2, COX-2 and beta-catenin.Cell communication and signaling : CCS · 2021Article
- Role of apoptosis repressor with caspase recruitment domain (ARC) in cell death and cardiovascular disease.Apoptosis : an international journal on programmed cell death · 2021Review
- RNA-Seq Reveals Different Gene Expression in Liver-Specific Prohibitin 1 Knock-Out Mice.Frontiers in physiology · 2021Article
- Ras Signaling in Breast Cancer.Advances in experimental medicine and biology · 2021Article
- Molecular Characterization and Clinical Relevance of RNA Binding Proteins in Colorectal Cancer.Frontiers in genetics · 2020Article
- Role of apoptosis repressor with caspase recruitment domain (ARC) in cancer.Oncology letters · 2019Review
- Insulin-like growth factor 1/insulin-like growth factor 1 receptor signaling protects against cell apoptosis through the PI3K/AKT pathway in glioblastoma cells.Experimental and therapeutic medicine · 2018Article
- The role of apoptosis repressor with a CARD domain (ARC) in the therapeutic resistance of renal cell carcinoma (RCC): the crucial role of ARC in the inhibition of extrinsic and intrinsic apoptotic signalling.Cell communication and signaling : CCS · 2017Article
- Expression of the apoptosis repressor with caspase recruitment domain (ARC) in liver metastasis of colorectal cancer and its correlation with DNA mismatch repair proteins and p53.Journal of cancer research and clinical oncology · 2016Article
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- A novel role for the apoptosis inhibitor ARC in suppressing TNFα-induced regulated necrosis.Cell death and differentiation · 2014Article
- Apoptosis repressor with caspase recruitment domain is regulated by MAPK/PI3K and confers drug resistance and survival advantage to AML.Apoptosis : an international journal on programmed cell death · 2014Article
- The apoptosis repressor with a CARD domain (ARC) gene is a direct hypoxia-inducible factor 1 target gene and promotes survival and proliferation of VHL-deficient renal cancer cells.Molecular and cellular biology · 2014Article
- The apoptosis inhibitor ARC alleviates the ER stress response to promote β-cell survival.Diabetes · 2013Article
- cis-Expression QTL analysis of established colorectal cancer risk variants in colon tumors and adjacent normal tissue.PloS one · 2012Article
- Apoptosis inhibitor ARC promotes breast tumorigenesis, metastasis, and chemoresistance.Cancer research · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Inhibition of apoptosis is critical for carcinogenesis. ARC (apoptosis repressor with caspase recruitment domain) is an endogenous inhibitor of apoptosis that antagonizes both intrinsic and extrinsic apoptosis pathways. Although normally expressed in striated myocytes and neurons, ARC is markedly induced in a variety of primary human epithelial cancers and renders cancer cells resistant to killing. The mechanisms that mediate the induction of ARC in cancer are unknown. Herein we demonstrate that increases in ARC abundance are stimulated by Ras through effects on transcription and protein stability. Overexpression of activated N-Ras or H-Ras in normal cells is sufficient to increase ARC mRNA and protein levels. Similarly, transgenic expression of activated H-Ras induces ARC in both the normal mammary epithelium and resulting tumors of intact mice. Conversely, knockdown of endogenous N-Ras in breast and colon cancer cells significantly reduces ARC mRNA and protein levels. The promoter of the Nol3 locus, encoding ARC, is activated by N-Ras and H-Ras in a MEK/ERK-dependent manner. Ras also stabilizes ARC protein by suppressing its polyubiquitination and subsequent proteasomal degradation. In addition to the effects of Ras on ARC abundance, ARC mediates Ras-induced cell survival and cell cycle progression. Thus, Ras induces ARC in epithelial cancers, and ARC plays a role in the oncogenic actions of Ras.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.