ArticleActa pharmacologica Sinica2011
Depletion of insulin receptor substrate 2 reverses oncogenic transformation induced by v-src.
Article in Acta pharmacologica Sinica, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 3 citations in OpenAlex.
- Aflatoxin B1 induces Src phosphorylation and stimulates lung cancer cell migration.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Src tyrosine kinase signaling antagonizes nuclear localization of FOXO and inhibits its transcription factor activity.Scientific reports · 2014Article
- Tanshinone-1 induces tumor cell killing, enhanced by inhibition of secondary activation of signaling networks.Cell death & disease · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the role of insulin receptor substrate 2 (IRS-2) in oncogenic transformation induced by v-src.
methodsIRS-2 gene was silenced using small interfering RNAs (siRNAs). Nuclear translocation and interaction of IRS-2 with v-src was determined using subcellular fractionation, confocal microscopy, and immunoprecipitation. The activity of the cyclin D1 promoter and r-DNA promoter was measured with a luciferase assay.
resultsDepletion of IRS-2 inhibited R-/v-src cell growth and reverse the oncogenic transformation. IRS-2 bound to src via its two PI3-K binding sites, which are critical for activities involved in the transformation. Nuclear IRS-2 occupied the cyclin D1 and rDNA promoters. The combination of IRS-2 and v-src increased the activity of the two promoters, especially the rDNA promoter.
conclusionDepletion of insulin receptor substrate 2 could reverse oncogenic transformation induced by v-src.
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Registered trials
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