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Depletion of insulin receptor substrate 2 reverses oncogenic transformation induced by v-src

  
@article{APS5474,
	author = {Hong-zhi Sun and Lin Xu and Bo Zhou and Wei-jin Zang and Shu-fang Wu},
	title = {Depletion of insulin receptor substrate 2 reverses oncogenic transformation induced by v-src},
	journal = {Acta Pharmacologica Sinica},
	volume = {32},
	number = {5},
	year = {2016},
	keywords = {},
	abstract = {Aim: To investigate the role of insulin receptor substrate 2 (IRS-2) in oncogenic transformation induced by v-src.
 Methods: IRS-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.
 Results: Depletion 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.
 Conclusion: Depletion of insulin receptor substrate 2 could reverse oncogenic transformation induced by v-src.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/5474}
}