Gene interactions and pathways from curated databases and text-mining

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BCL2 — PTGS2

Text-mined interactions from Literome

Sun et al., Cancer Res 2002 (Colonic Neoplasms) : COX-2 mediated up-regulation of Bcl-2 suggests a potential mechanism for reduced apoptotic susceptibility
Wikström et al., Biochem Biophys Res Commun 2003 : Furthermore, COX-2 activity is responsible for the effects on Bcl-2 , but this is not conveyed through the production of PGE ( 2 )
Konturek et al., Dig Dis Sci 2003 (Helicobacter Infections...) : ( 5 ) Vioxx also enhanced expression of COX-2 , PPARy, Bax, and caspase-3, while inhibiting the expression of Bcl-2 and survivin, suggesting that COX-2 blockade might be useful in chemoprevention against gastric cancer possibly due to enhancement of the PPARy- and proapoptotic proteins dependent apoptosis and the reduction in progastrin/gastrin induced promotion of tumor growth
Tari et al., Lab Invest 2005 (Breast Neoplasms) : However, we did not observe any changes in Bcl-2, Bcl-XL , or Bax expression induced by COX-2 or PGE2
Konturek et al., Dig Dis Sci 2006 (Adenocarcinoma...) : We conclude that ( 1 ) distal CRC patients show significantly higher serum progastrin levels than matched healthy controls, confirming that this hormone may be implicated in rectal carcinogenesis ; ( 2 ) CRC patients exhibit significantly higher serum levels of IL-8 and TNF-alpha than healthy controls, probably reflecting more widespread inflammatory reaction in the colonic mucosa in CRC ; ( 3 ) gastrin, COX-2, Bcl-2, survivin, and NFkappa B were overexpressed in CRC tumor compared to intact mucosa, but treatment with CLX significantly reduced serum levels of progastrin and IL-8 and TNF-alpha, which could mediate the up-regulation of COX-2 in CRC ; and ( 4 ) CLX also enhanced expression of COX-2 , while inhibiting the expression of gastrin, Bcl-2 , survivin, and NFkappa B, suggesting that COX-2 inhibition might be useful in chemoprevention against CRC, possibly due to suppression of the antiapoptotic proteins and reduction in progastrin induced and NFkappa B-promoted tumor growth
Liu et al., Ann Hematol 2007 (Leukemia) : Taken together, our results demonstrate for the first time that downregulation of cyclooxygenase-2 expression, disruption of mitochondrial membrane potential, activation of caspase-3, downregulation of Bcl-2, Bcl-Xl , and Mcl-1, and upregulation of Bax are involved in PPAR-gamma agonists induced apoptosis in these two human monocyte leukemia cells
Liu et al., Dig Dis Sci 2009 (Stomach Neoplasms) : The present study shows that celecoxib causes growth inhibition of gastric carcinoma cells by decreasing Bcl-2 of cyclooxygenase-2 dependent pathway, and by increasing p21 ( WAF1 ) and p27 ( KIP1 ) of cyclooxygenase-2 independent pathway
Chen et al., Clin Cancer Res 2010 (Carcinoma, Hepatocellular...) : Furthermore, using the shRNA and transgene coexpression adenovirus system, we showed that silencing of COX-2 increased the sensitivity of hepatocellular carcinoma to TRAIL through inhibition of Bcl-2 and Bcl-w
Kim et al., Korean journal of urology 2011 : Chronic inflammation in BPH causes an overexpression of COX-2 , which induces the increased expression of Bcl-2 and VEGF