Gene interactions and pathways from curated databases and text-mining

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AKT1 — MMP9

Text-mined interactions from Literome

Thant et al., Clin Exp Metastasis 2000 (Neoplasm Invasiveness...) : Taken together, our results suggest that activation of dual signaling pathways, MEKI-MAPK and P13K-Akt , is required for the FN-dependent activation of MMP-9 secretion
Kim et al., FASEB J 2001 (Neoplasm Invasiveness) : The increase in MMP-9 production was mediated by activation of nuclear factor-kappaB transcriptional activity by Akt/PKB
O-charoenrat et al., Int J Cancer 2004 (Carcinoma, Squamous Cell...) : Taken together, our data show that BTC induces MMP-9 production and invasion primarily through activation of EGFR, MAPK and PI3K/Akt in HNSCC cells
Hsieh et al., Cell Signal 2004 (MAP Kinase Signaling System) : Taken together, these results suggest that in RBA cells, activation of p42/p44 MAPK and Akt cascades mediated through NF-kappaB pathway are essential for BK-induced MMP-9 gene expression
Lu et al., J Leukoc Biol 2005 : The mechanism by which Akt regulates MMP-9 is through the activation of NF-kappaB, as shown by coimmunoprecipitation of the phosphorylated form of IKKalpha and Akt as well as the SH-5 suppression of the dissociation of IkappaB from NF-kappaB and the activation of NF-kappaB p65
Fukaya et al., Oncol Rep 2005 (Lung Neoplasms...) : Inhibition of PI3K-Akt signaling in LM8 by a PI3K inhibitor, LY294002, or by a dominant negative form of Akt, resulted in suppression of MMP secretion, in vitro invasiveness, cell locomotion and in vivo pulmonary metastasis ... In contrast, expression of an active form of Akt in Dunn substantially activated its MMP secretion, in vitro invasiveness, cell locomotion and in vivo pulmonary metastasis
Lim et al., FEBS Lett 2006 : CpG ODN induced the phosphorylation of Akt, and the inhibition of Akt by LY294002 suppressed CpG ODN induced TNF-alpha, TNFR-II, and MMP-9 expressions
Van Themsche et al., J Biol Chem 2007 (Endometrial Neoplasms...) : In addition, using RNA interference and pharmacological inhibitors, we show that TGF-beta increases cellular invasiveness via two distinct signaling pathways in endometrial carcinoma cells : phosphatidylinositol 3-kinase/AKT dependent up-regulation of XIAP and protein kinase C-dependent induction of matrix-metalloproteinase-9 (MMP-9) expression
Liau et al., Cancer Res 2006 (Adenocarcinoma...) : Akt dependent modulation of MMP-9 activity contributed significantly to HMGA1 overexpression induced increases in invasive capacity
Srivastava et al., J Biol Chem 2007 : Inhibition of Akt also inhibited the TNF-alpha induced production of MMP-9
Mantuano et al., J Neurosci 2008 (Sciatic Neuropathy) : Herein, we demonstrate that MMP-9 activates extracellular-signal regulated kinase ( ERK1/2 ) and Akt in Schwann cells in culture
Kim et al., Exp Mol Med 2009 : A chemical inhibitor of MEK1/2 or PI3K reduced phosphorylation of ERK or Akt , respectively, and also inhibited CSE mediated MMP-9 induction
Anggakusuma et al., J Dermatol Sci 2010 (Inflammation) : These results suggest that macelignan protects skin keratinocytes from UVB induced damage and inhibits MMP-9 and COX-2 expression by attenuating the activation of MAPKs and PI3K/Akt
Liu et al., Am J Respir Cell Mol Biol 2010 (Carcinoma, Non-Small-Cell Lung...) : We also demonstrated that phosphoinositide 3-kinase/Akt and NF-?B related pathways contributed to the HMGB1 induced MMP-9 expression and cellular metastatic ability
Li et al., Phytomedicine 2010 (Hyperplasia) : However, HG-down regulated MT-1 MMP expression was independent of activation of ERK1/2 and Akt when using their inhibitors of DB98059 ( ERK1/2 ) and LY294002 ( Akt ) alone or in combination
Kim et al., Biochim Biophys Acta 2010 (Prostatic Neoplasms) : Collectively, these data in a mouse prostate cell system uncover for the first time a novel and complex relationship between PTEN loss mediated PI3K/AKT activation and posttranslational regulation of MT1-MMP , which may play a role in PC progression
Guan et al., Acta Neurochir Suppl (Wien) 2011 (Brain Infarction...) : Mechanisms identified include inhibition of MMP-9 , activation of Akt , and increased expression of proangiogenic growth factors
Yoo et al., Cancer Res 2011 (Lymphatic Metastasis...) : Mechanistic investigations revealed that phosphoinositide 3-kinase (PI3K)/Akt inhibition blocked Shh induced epithelial-mesenchyme transition, the activity of matrix metalloproteinase 9 (MMP-9) , and lymphangiogenesis, reducing tumor invasiveness and metastasis
Yang et al., Journal of neuroinflammation 2012 : JEV induced MMP-9 expression and promoter activity were inhibited by pretreatment with inhibitors of AP-1 ( tanshinone ), c-Src ( PP1 ), PDGFR ( AG1296 ), and PI3K ( LY294002 ), and by transfection with siRNAs of c-Jun, c-Fos, PDGFR, and Akt
Wang et al., Biochem Biophys Res Commun 2012 (Vitreoretinopathy, Proliferative) : TNF-a promotes human retinal pigment epithelial (RPE) cell migration by inducing matrix metallopeptidase 9 (MMP-9) expression through activation of Akt/mTORC1 signaling ... Suppression Akt/mTOR complex 1(mTORC1) activation by LY 294002 and rapamycin inhibited TNF-a mediated MMP-9 expression
Ahmad et al., Mol Cell Endocrinol 2012 : Studies using chemical inhibitors and siRNAs to signaling molecules showed that PI3K, Akt , ERK and PKC-? and the transcription factors Elk-1, c-fos and, to a lesser extent, NF-?B are involved in relaxin 's induction of MMP-9
Chen et al., Carcinogenesis 2013 (Liver Neoplasms...) : Further investigations showed that activation of AKT and FAK were required for rSHH-N mediated upregulation of MMP-2 and MMP-9 , cell migration and invasion
Yano et al., Cell communication and signaling : CCS 2012 : PI3K/Akt dependent activation of cAMP responsive element binding protein ( CREB)-1 induced expression of matrix metalloproteinase (MMP)-9 and suppressing MMP activity by doxycycline partially reversed FN accumulation in the InsR silenced cells
Shen et al., Circ Res 2013 (Aneurysm, Dissecting...) : In cultured human aortic vascular smooth muscle cells, AKT2 inhibited the expression of MMP-9 and stimulated the expression of TIMP-1 by preventing the binding of transcription factor forkhead box protein O1 to the MMP-9 and TIMP-1 promoters