Gene interactions and pathways from curated databases and text-mining

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BCL2 — STAT3

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Rebbaa et al., Mol Med 2001 (Neuroblastoma) : Up-regulation of Stat3 phosphorylation and Bcl-xL expression, increased nuclear translocation of phospho-Stat3 , and binding to DNA occurred only in resistant SKN-SH/Dox6 cells
Schweizer et al., J Cell Biol 2002 (Facial Nerve Injuries) : Stat3 is essential for upregulation of Reg-2 and Bcl-xl expression in lesioned motoneurons
Yoshida et al., J Exp Med 2002 (Cell Transformation, Neoplastic...) : Activation of STAT3 by the HCV core in NIH-3T3 cells resulted in rapid proliferation and up-regulation of Bcl-XL and cyclin-D1
Real et al., Oncogene 2002 (Brain Neoplasms...) : Resistance to chemotherapy via Stat3 dependent overexpression of Bcl-2 in metastatic breast cancer cells ... Furthermore, transfection of 435B with a dominant negative Stat3 markedly reduced the expression of Bcl-2 protein, whereas transient expression of a constitutively active Stat3 increased Bcl-2 in parental 435 cells
Moodley et al., Am J Respir Cell Mol Biol 2003 (MAP Kinase Signaling System...) : Using RNase protection assays, we showed that IL-6 enhanced Fas induced apoptosis and expression of Bax in normal-Fb, but inhibited apoptosis and induced expression of Bcl-2 in IPF-Fb. Densitometry of Western blots revealed a Bcl-2/Bax ratio 0.15 +/- 0.01 in normal-Fb compared with 12.05 +/- 1.0 in IPF-Fb. Upregulation of Bcl-2 in normal-Fb and Bax in IPF-Fb were both STAT-3 dependent
Konnikova et al., BMC cancer 2003 (Astrocytoma) : Moreover, STAT3 is required for the expression of the antiapoptotic genes survivin and Bcl-xL in the A172 glioblastoma cell line
Rust et al., J Pathol 2005 (Lymphoma, Large B-Cell, Diffuse) : Activated STAT3 leads to the induction of several genes such as Mcl-1, Bcl-2 and Bcl-X ( L ), and tissue inhibitor of metalloproteinase ( TIMP ) -1
Bhattacharya et al., Biochem J 2005 : STAT3 mediated transcription of Bcl-2 , Mcl-1 and c-IAP2 prevents apoptosis in polyamine depleted cells ... These results suggest that activation of STAT3 in response to polyamine depletion increases the transcription and subsequent expression of anti-apoptotic Bcl-2 and IAP family proteins and thereby promotes survival of cells against TNF-alpha induced apoptosis
Akasaki et al., J Biol Chem 2006 (Glioma) : Reduction of pY705-STAT3 in glioma cells caused down-regulation of FLIP ( FADD-like IL-1beta converting enzyme-inhibitory protein ) and Bcl-2
Lu et al., J Biol Chem 2006 : Not only the up-regulation of p50alpha and p55alpha but also the repression of cyclin D1 and Bcl-2 in SOCS3 ( -/- ) MEFs was inhibited by dominant negative STAT3
Kim et al., Mol Endocrinol 2007 (Carcinoma, Papillary...) : Chromatin immunoprecipitation studies indicate that expression of LKB1 reduces the binding of STAT3 to its target promoters and suppresses STAT3 mediated expression of Cyclin D1, VEGF, and Bcl-xL
Lee et al., Int J Cancer 2008 (Carcinoma, Squamous Cell...) : A signal network involving coactivated NF-kappaB and STAT3 and altered p53 modulates BAX/BCL-XL expression and promotes cell survival of head and neck squamous cell carcinomas
Delgado et al., Dig Dis Sci 2008 (Adenocarcinoma...) : This drug significantly reduced the up-regulations of cyclin D1, cyclin E, c-Myc, and Bcl-2 as well as the activation of STAT3 in SEG-1 cells
Chen et al., Cancer Biol Ther 2008 (Neoplasms...) : Activated STAT3 mediated VEGF induction of EC Bcl-2 and contributed to VEGF protection of EC from apoptosis
Marrero et al., Brain Res 2009 (Inflammation) : In this study, we investigated the effects of inhibiting the alpha7 nAChR-JAK2 pro-survival cascade on the nicotine induced production of the survival factor Bcl-2 and the transcriptional activation of NF-kappaB, AP-1, STAT1, STAT3 , and STAT5
Choi et al., Exp Mol Med 2009 : STAT3 is involved in phosphatidic acid induced Bcl-2 expression in HeLa cells ... Furthermore, STAT3 siRNA treatments inhibited PA-induced Bcl-2 expression, suggesting that STAT3 ( Ser727 ) is involved in PA-induced Bcl-2 expression
Chen et al., J Mol Neurosci 2010 (Brain Neoplasms...) : In addition, down-regulation of Stat3 can suppress the expression of MMP-2, Bcl-xL and survivin but not 67LR
Glienke et al., Tumour Biol 2011 (Pancreatic Neoplasms) : siRNA targeting STAT3 was used to evaluate the role of STAT3 in modulating the expression of Survivin/BIRC5 and BCL-xL in the pancreatic cancer cell lines PANC-1 and BxPC-3 and induction of apoptosis
Zhao et al., Cytokine 2011 (Brain Injuries) : Moreover, AG490 attenuated rhEPO 's neuroprotection by down regulating rhEPO induced activation of JAK2/STAT3 , and inhibiting Bcl-2 and Bcl-xl
Sun et al., Journal of translational medicine 2012 : Down regulation of STAT-3 with siRNA resulted in a reduced expression of Bcl-2 and cyclin D1
Zhang et al., Proc Natl Acad Sci U S A 2012 (Breast Neoplasms...) : BP-1-102 mediated inhibition of aberrantly active Stat3 in tumor cells suppresses the expression of c-Myc, Cyclin D1, Bcl-xL , Survivin, VEGF, and Krüppel-like factor 8, which is identified as a Stat3 target gene that promotes Stat3 mediated breast tumor cell migration and invasion
Tu et al., Cancer Lett 2012 (Bone Neoplasms...) : The inhibition of STAT3 in Saos-2 cells by siRNA or AG490 decreased cell proliferation, migration and invasion, down-regulated the mRNA expression of Cyclin D, Bcl-xL and Survivin and enhanced the apoptotic response
Zgheib et al., Eur Cytokine Netw 2012 (Cardiomegaly...) : Different effects of LIF were seen in protein levels of genes associated with STAT3 in the left ventricle : levels of SOD2 and Bcl-xL were unchanged, but levels of total STAT3 and MCP-1 were increased
Zhang et al., Cell Biol Int 2013 : Both Bcl-2 and Mcl-1 in ADAM8 overexpressing A549 cells were profoundly diminished by STAT3 knockdown
Khan et al., BioMed research international 2013 (Liver Neoplasms) : This alantolactone induced apoptosis was found to be associated with GSH depletion, inhibition of STAT3 activation, ROS generation, mitochondrial transmembrane potential dissipation, and increased Bax/Bcl-2 ratio and caspase-3 activation