ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010
Retinoblastoma cells are inhibited by aminoimidazole carboxamide ribonucleotide (AICAR) partially through activation of AMP-dependent kinase.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- The role of AMPK in cancer metabolism and its impact on the immunomodulation of the tumor microenvironment.Frontiers in immunology · 2023Review
- Multienzyme interactions of the de novo purine biosynthetic protein PAICS facilitate purinosome formation and metabolic channeling.The Journal of biological chemistry · 2022Article
- Article
- The Role of Intraarterial Chemotherapy in the Management of Retinoblastoma.Journal of ophthalmology · 2020Review
- An update on PTEN modulators - a patent review.Expert opinion on therapeutic patents · 2019Review
- Article
- AICAR suppresses TNF-α-induced complement factor B in RPE cells.Scientific reports · 2017Article
- 5-Aminoimidazole-4-carboxamide ribonucleoside-mediated adenosine monophosphate-activated protein kinase activation induces protective innate responses in bacterial endophthalmitis.Cellular microbiology · 2016Article
- CaMKK2 Suppresses Muscle Regeneration through the Inhibition of Myoblast Proliferation and Differentiation.International journal of molecular sciences · 2016Article
- Effects of metformin on retinoblastoma growth in vitro and in vivo.International journal of oncology · 2014Article
- The clinically used photosensitizer Verteporfin (VP) inhibits YAP-TEAD and human retinoblastoma cell growth in vitro without light activation.Experimental eye research · 2014Article
- Uveal melanoma cell growth is inhibited by aminoimidazole carboxamide ribonucleotide (AICAR) partially through activation of AMP-dependent kinase.Investigative ophthalmology & visual science · 2014Article
- MicroRNA-21 Down-regulates Rb1 Expression by Targeting PDCD4 in Retinoblastoma.Journal of Cancer · 2014Article
- Article
- Regulation of ion channels and transporters by AMP-activated kinase (AMPK).Channels (Austin, Tex.) · 2014Review
- AMP-dependent kinase inhibits oxidative stress-induced caveolin-1 phosphorylation and endocytosis by suppressing the dissociation between c-Abl and Prdx1 proteins in endothelial cells.The Journal of biological chemistry · 2013Article
- Acadesine Triggers Non-apoptotic Death in Tumor Cells.Acta naturae · 2013Article
- Article
- Retinoblastoma: Recent trends A mini review based on published literature.Oman journal of ophthalmology · 2011Article
- Activation of AMP-activated protein kinase prevents lipotoxicity in retinal pericytes.Investigative ophthalmology & visual science · 2011Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
5-Aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR), an analog of AMP, is widely used as an activator of AMP-kinase (AMPK), a protein that regulates the responses of the cell to energy change. We studied the effects of AICAR on the growth of retinoblastoma cell lines (Y79, WERI, and RB143). AICAR inhibited Rb cell growth, induced apoptosis and S-phase cell cycle arrest, and led to activation of AMPK. These effects were abolished by treatment with dypiridamole, an inhibitor that blocks entrance of AICAR into cells. Treatment with the adenosine kinase inhibitor 5-iodotubericidin to inhibit the conversion of AICAR to ZMP (the direct activator of AMPK) reversed most of the growth-inhibiting effects of AICAR, indicating that some of the antiproliferative effects of AICAR are mediated through AMPK activation. In addition, AICAR treatment was associated with inhibition of the mammalian target of rapamycin pathway, decreased phosphorylation of ribosomal protein-S6 and 4E-BP1, down-regulation of cyclins A and E, and decreased expression of p21. Our results indicate that AICAR-induced activation of AMPK inhibits retinoblastoma cell growth. This is one of the first descriptions of a nonchemotherapeutic drug with low toxicity that may be effective in treating Rb patients.
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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.