We are analyzing https://link.springer.com/article/10.1007/s00384-004-0616-2.

Title:
Bile salt-induced apoptosis in human colon cancer cell lines involves the mitochondrial transmembrane potential but not the CD95 (Fas/Apo-1) receptor | International Journal of Colorectal Disease
Description:
Background and aims Depending on their physico-chemical characteristics, bile acids can be potent inducers of apoptosis in colon cancer cells. This observation contrasts with bile acids being promoters of colorectal cancer carcinogenesis. Our recent observation of caspase activation in deoxycholate (DC)-treated colon cancer cell lines prompted us to analyze the mechanisms of bile acid-induced colon cancer cell death. Methods CD95 expression was correlated to DC-induced cell death in four colon cancer cell lines. Mitochondrial transmembrane potential (MTP) was determined in whole cells as well as in isolated mitochondria. Results On 2 of the 4 human colon cancer cell lines investigated, no CD95 was detected. These data were supported by a lack of CD95 mRNA in those cell lines that did not express CD95 on their surface. The apoptotic response to bile acids did not correlate with CD95 receptor expression on the respective cell lines. Therefore, we analyzed the MTP after the addition of toxic bile acids. MTP was destabilized early after the addition of deoxycholate to SW480 cells. These data were confirmed in isolated mitochondria, which showed strong swelling after the addition of DC. Accordingly, release of cytochrome-c from the mitochondrial intermembrane space into the cytosol, indicating dissipation of the MTP, and subsequent caspase-3 cleavage were detectable as early as 3 min after the addition of DC. Conclusion In contrast to hepatocytes and hepatic carcinoma cell lines, DC induces apoptosis in colon cancer cell lines via a CD95 receptor-independent mechanism. Direct induction of the mitochondrial permeability transition by toxic bile acids is suggested as the apoptosis-inducing mechanism in colon cancer cells.
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Topics {✒️}

bile duct ligation spivey jr bile salt-induced apoptosis bile-salt-induced apoptosis ngf/tnf receptor superfamily month download article/chapter dc-induced cell death promote anti-tumour phenotypes apaf-1/caspase-9 complex initiates ruth knüchel-clarke colon cancer cells toxic bile acids article international journal colon cancer risk escape cd95-mediated apoptosis cell death control mitochondrial transmembrane potential secondary bile acids dietary bile acids colon carcinoma cells colorectal cancer carcinogenesis full article pdf respective cell lines aberrant crypt foci bile salt deoxycholate cd95 receptor-independent mechanism privacy choices/manage cookies german research foundation colorectal disease aims neoplastic colon epithelium mitochondrial permeability transition matrix calcium level bile acid fas death pathway colorectal tumour cells cell death mouse involves fas hepatic mitochondrial lipids universidade de lisboa check access instant access anti-fas antibody mitochondrial intermembrane space mitochondrial pyruvate carboxylation bile acids apoptotic protease cascade potential biological marker klaus schlottmann subsequent caspase-3 cleavage colon carcinogenesis

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         description:Depending on their physico-chemical characteristics, bile acids can be potent inducers of apoptosis in colon cancer cells. This observation contrasts with bile acids being promoters of colorectal cancer carcinogenesis. Our recent observation of caspase activation in deoxycholate (DC)-treated colon cancer cell lines prompted us to analyze the mechanisms of bile acid-induced colon cancer cell death. CD95 expression was correlated to DC-induced cell death in four colon cancer cell lines. Mitochondrial transmembrane potential (MTP) was determined in whole cells as well as in isolated mitochondria. On 2 of the 4 human colon cancer cell lines investigated, no CD95 was detected. These data were supported by a lack of CD95 mRNA in those cell lines that did not express CD95 on their surface. The apoptotic response to bile acids did not correlate with CD95 receptor expression on the respective cell lines. Therefore, we analyzed the MTP after the addition of toxic bile acids. MTP was destabilized early after the addition of deoxycholate to SW480 cells. These data were confirmed in isolated mitochondria, which showed strong swelling after the addition of DC. Accordingly, release of cytochrome-c from the mitochondrial intermembrane space into the cytosol, indicating dissipation of the MTP, and subsequent caspase-3 cleavage were detectable as early as 3 min after the addition of DC. In contrast to hepatocytes and hepatic carcinoma cell lines, DC induces apoptosis in colon cancer cell lines via a CD95 receptor-independent mechanism. Direct induction of the mitochondrial permeability transition by toxic bile acids is suggested as the apoptosis-inducing mechanism in colon cancer cells.
         datePublished:2004-09-07T00:00:00Z
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            Apoptosis
            CD95
            Colon cancer
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            Surgery
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      headline:Bile salt-induced apoptosis in human colon cancer cell lines involves the mitochondrial transmembrane potential but not the CD95 (Fas/Apo-1) receptor
      description:Depending on their physico-chemical characteristics, bile acids can be potent inducers of apoptosis in colon cancer cells. This observation contrasts with bile acids being promoters of colorectal cancer carcinogenesis. Our recent observation of caspase activation in deoxycholate (DC)-treated colon cancer cell lines prompted us to analyze the mechanisms of bile acid-induced colon cancer cell death. CD95 expression was correlated to DC-induced cell death in four colon cancer cell lines. Mitochondrial transmembrane potential (MTP) was determined in whole cells as well as in isolated mitochondria. On 2 of the 4 human colon cancer cell lines investigated, no CD95 was detected. These data were supported by a lack of CD95 mRNA in those cell lines that did not express CD95 on their surface. The apoptotic response to bile acids did not correlate with CD95 receptor expression on the respective cell lines. Therefore, we analyzed the MTP after the addition of toxic bile acids. MTP was destabilized early after the addition of deoxycholate to SW480 cells. These data were confirmed in isolated mitochondria, which showed strong swelling after the addition of DC. Accordingly, release of cytochrome-c from the mitochondrial intermembrane space into the cytosol, indicating dissipation of the MTP, and subsequent caspase-3 cleavage were detectable as early as 3 min after the addition of DC. In contrast to hepatocytes and hepatic carcinoma cell lines, DC induces apoptosis in colon cancer cell lines via a CD95 receptor-independent mechanism. Direct induction of the mitochondrial permeability transition by toxic bile acids is suggested as the apoptosis-inducing mechanism in colon cancer cells.
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         Apoptosis
         CD95
         Colon cancer
         Mitochondrial transmembrane potential
         Surgery
         Internal Medicine
         Gastroenterology
         Hepatology
         Proctology
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