Gene interactions and pathways from curated databases and text-mining

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PIK3CA — STAT3

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Alonzi et al., Mol Cell Neurosci 2001 : To assess the relative importance of these pathways in promoting the survival of cytokine dependent neurons, we conditionally inactivated STAT3 in mice and inhibited MEK, PI3K , and Akt in cultured neurons using pharmacological reagents and by expressing specific inhibitory proteins
Niculescu et al., Immunol Res 2001 : PI3-K activation by C5b-9 induced STAT3 phosphorylation and translocation from cytoplasm to nucleus
Fung et al., Cell Signal 2003 : IL-2 activation of a PI3K dependent STAT3 serine phosphorylation pathway in primary human T cells ... However, the coupling of STAT3 serine phosphorylation to PI3K in response to IL-2 has yet to be shown in either T cell lines or primary human T cells
Tian et al., Acta Pharmacol Sin 2004 (Cardiomegaly) : The hypertrophic effect of CT-1 was essentially mediated by STAT3 , independent of PI3-K , and negatively regulated by ERK1/2 via inhibiting the phosphorylation of STAT3
Abell et al., Nat Cell Biol 2005 : Here we show that expression of the PI(3)K regulatory subunits p55alpha and p50alpha is induced by Stat3 during involution ... We propose a novel mechanism in which Stat3 regulates apoptosis by inducing expression of distinct PI(3)K regulatory subunits to downregulate PI(3)K-Akt mediated survival signalling
Kok et al., Trends Biochem Sci 2009 (Neoplasms) : Recently identified mechanisms that control PI3K production include increased gene copy number in cancer, and transcriptional regulation of the p110alpha PI3K gene by FOXO3a, NF-kappaB and p53, and of the PI3K regulatory subunits by STAT3 , EBNA-2 and SREBP ... Recently identified mechanisms that control PI3K production include increased gene copy number in cancer, and transcriptional regulation of the p110alpha PI3K gene by FOXO3a, NF-kappaB and p53, and of the PI3K regulatory subunits by STAT3 , EBNA-2 and SREBP
Lin et al., Toxicon 2010 (Breast Neoplasms) : Moreover, the PI3K inhibitor wortmannin blocked activation of STAT3 and Akt without affecting the JAK2 activation, whereas JAK2 inhibitor AG490 suppressed the levels of phospho-STAT3, phospho-Akt, and PI3K, suggesting that PI3K activation occurs after JAK2 phosphorylation, and both PI3K and JAK2 kinases cooperate to mediate STAT3 and Akt phosphorylation
Su et al., Clin Exp Pharmacol Physiol 2010 : These observations suggest that PI3-K is an upstream activator of JAK2/STAT3
Wang et al., J Immunol 2011 : IFN-ß increased the phosphorylated levels of CREB and STAT3 but only CREB levels were affected by PI3K
Bito et al., Journal of skin cancer 2011 : Furthermore, a PI3K inhibitor also suppressed Stat3 activation in HSC-1 cells to some degree ... These data suggest that Stat3 activation through EGFR and/or PI3K/Akt activation plays a critical role in the proliferation and survival of human cutaneous SCC
Hart et al., Proc Natl Acad Sci U S A 2011 (Cell Transformation, Neoplastic) : GDC-0941, a specific inhibitor of PI3K reduces the level of Stat3 phosphorylation ... The effect of PI3K on Stat3 appears to be mediated by a member of the Tec kinase family ... In some human tumor cell lines, the enhanced phosphorylation of Stat3 is inhibited by both PI3K and by Tec kinase inhibitors, suggesting that the link between PI3K and Stat3 is significant in human cancer
Sahu et al., J Neuroendocrinol 2013 : In the hypothalamus, leptin stimulates STAT3 activation, and induces PI3K and PDE3B activities, among others
Pijet et al., Cytokine 2013 (MAP Kinase Signaling System) : Detailed acute and chronic studies with the use of metabolic inhibitors revealed that both JAK/STAT3 and MEK/MAPK but not PI3-K/AKT/GSK-3ß signaling pathways were activated by leptin, and that STAT3 ( Y ( 705 ) P-STAT3 ) and MEK ( T ( 202/ ) Y ( 204 ) P-ERK1/2 ) mediate these effects