INT73593
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
OBJECTIVE: To determine the Bcl-2 and Bax expressions in endometriotic and adenomyotic tissues. | |||||||||||||||
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Bcl-2 and Bax expression in human endometriotic and adenomyotic tissues. | |||||||||||||||
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Bcl-2 and Bax expressions were investigated on 56 formalin-fixed and paraffin-embedded tissue by immunohistochemical staining and electron microscopy. | |||||||||||||||
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RESULTS: In normal pancreas and chronic pancreatitis tissues, bcl-2, bax and bcl-x were predominantly expressed in ductal epithelial cells while p53 was not detected. | |||||||||||||||
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Detailed tissue expression of bcl-2, bax, bak and bcl-x in the normal human pancreas and in chronic pancreatitis, ampullary and pancreatic ductal adenocarcinomas. | |||||||||||||||
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We observed that IR-induced bax and p21(WAF1/Cip1) protein expression were attenuated selectively in normal stromal and epithelial cell cultures, yet maintained their p53-dependency in malignant cell lines. | |||||||||||||||
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The expression of p53, p21, bax and caspase-3 increased in Tan-I-treated cells. | |||||||||||||||
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The expression of bcl-2 and bax was analyzed by Western blot analysis. | |||||||||||||||
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To clarify the basis for cell killing during prostate cancer radiotherapy, we determined the IR-induced expression of several apoptotic- (bax, bcl-2, survivin and PARP) and G1-cell cycle checkpoint- (p53 and p21(WAF1/Cip1)) related proteins, in both normal (PrEC-epithelial and PrSC-stromal) and malignant (LNCaP, DU-145 and PC-3; all epithelial) prostate cells. | |||||||||||||||
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RESULTS: Our results showed that aspisol reduced viability of MDA-MB-231 cells in time- and dose- dependent fashions and induced apoptosis by increase of caspase-3 and bax expressions while decrease of COX-2 and bcl-2 expression in vitro. | |||||||||||||||
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CONCLUSIONS: Our in vitro and in vivo data indicated that the antitumor effects of aspisol on breast cancer cells was probably mediated by the induction of apoptosis, and it could be linked to the downregulation of the COX-2 or bcl-2 expression and up-regulation of caspase-3 or bax expression.
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Ribonuclease protection assays compared the effects of acetaminophen and E2 on expression of selected genes (c-myc, c-fos, cyclin D1, bcl-2, bax, gadd45, mcl-1, p53, p21(CIP1/WAF1), and bcl-xL) in E2-responsive breast cancer (MCF-7) and endometrial adenocarcinoma (Ishikawa) cells as well as in E2-nonresponsive (MDA-MB-231) breast cancer cells. | |||||||||||||||
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Expression of cyclins B1, D3 and E and p21, p27, bax, bcl2 and cox-2 was studied immunohistochemically. | |||||||||||||||
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However the expression of apoptosis-related genes such as Fas, bcl-2 and bax was not affected by indomethacin. | |||||||||||||||
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This study focused on the biological mechanisms of sensitivity and resistance to NCX 4040, highlighting that the cytotoxic action of this drug may be due to the hyperexpression of Bax, its translocation to the mitochondria, the release of Cytochrome C, and the activation of caspases-9 and -3, overall in a p53-independent manner. | |||||||||||||||
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Morphine-treated Jurkat cells also showed a decreased expression of bcl-2 and an enhanced expression of bax. | |||||||||||||||
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Since Bax expression was stimulated only at high resveratrol concentrations while Bax translocation and mitochondria-mediated cell death were observed also at low concentrations, we asked what relevance Bax might have for the chemopreventive activity of the compound. | |||||||||||||||
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In other model systems, Bax was overproduced in response to drugs, including resveratrol [10,14]. | |||||||||||||||
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Concomitantly to the absence of apoptosis in those endometria, the pro-apoptotic gene bax mRNA abundance was unchanged during the menstrual cycle, at difference at the increase exhibited in normal endometrium, suggesting that the reduction of bax expression may be a mechanism that could explain the decreased incidence of apoptosis in endometriosis. | |||||||||||||||
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In agreement with these results, recent publications [3,34,35] also reported the absence of apoptotic cells and the increase of Bcl-2 and the reduction of Bax expression in eutopic endometrium from women with endometriosis, although Béliard et al. (2004) [4] were unable to find these differences between patients with endometriosis and normal women. | |||||||||||||||
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