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ji-ae shin & sung-dae cho suppressing cyclin-a2/akt/foxo3a signaling microarray-based expression profiling sung-dae cho eun-seon yoo month download article/chapter sung-hyun kim quantitative real-time pcr ros-erk-chop pathway vitro anti-cancer effects human oral cancer er stress oral cancer cells abt-263-mediated anticancer activity nam-pyo cho ji-ae shin �endoplasmic reticulum stress endoplasmic reticulum stress vivo anti-tumorigenic effects breast cancer cells author information authors full article pdf bh3-mimetic abt-737 bh3 mimetic abt-263 possesses anticancer potential kill cancer cells national research foundation privacy choices/manage cookies anti-apoptotic proteins oral pathology dental research institute related subjects fk506-induced apoptosis bh3-mimetic gossypol gossypol increases expression ji-youn jung /ebp-homologous protein /ebp homologous protein pro-apoptotic proteins abt-263 suppressed viability abt-263-treatead group abt-263 considerably enhanced abt-263-treated mice hepatocellular carcinoma cells antiapoptotic bcl-2 proteins oral cancer laboratory animal science tunel-positive cells check access instant access

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         headline:ABT-263 exhibits apoptosis-inducing potential in oral cancer cells by targeting C/EBP-homologous protein
         description:ABT-263 is a potent BH3 mimetic that possesses anticancer potential against various types of cancer. In general, this potential is due to its high binding affinity to anti-apoptotic proteins in the Bcl-2 family that disrupt sequestration of pro-apoptotic proteins. In the present study, we sought to identify an alternative regulatory mechanism responsible for ABT-263-mediated anticancer activity in human oral cancer. We investigated the in vitro anti-cancer effects of ABT-263 using a trypan blue exclusion assay, Western blotting, DAPI staining, immunofluorescence staining, a live/dead assay, microarray-based expression profiling, and quantitative real-time PCR. In vivo anti-tumorigenic effects of ABT-263 were examined using a nude mouse tumor xenograft model, a TUNEL assay, and immunohistochemistry. We found that ABT-263 suppressed viability and induced apoptosis in human oral cancer-derived cell lines HSC-3 and HSC-4. Subsequent microarray-based gene expression profiling revealed 55 differentially expressed genes in the ABT-263-treatead group, including 12 genes associated with “endoplasmic reticulum stress and apoptosis.” Consistent with the microarray results, the mRNA expression levels of the top four genes (CHOP, TRB3, ASNS, and STC2) were found to be significantly increased. In addition, we found that ABT-263 considerably enhanced the expression levels of the C/EBP-homologous protein (CHOP) and its mRNA, resulting in apoptosis induction in four other human oral cancer-derived cell lines (MC-3, YD-15, HN22, and Ca9.22). Extending our in vitro findings, we found that ABT-263 reduced the growth of HSC-4 cells in vivo at a dosage of 100 mg/kg/day without any change in body weight. TUNEL-positive cells were also found to be increased in tumors of ABT-263-treated mice without any apparent histopathological changes in liver or kidney tissues. These results provide evidence that ABT-263 may serve as an effective therapeutic agent for the treatment of human oral cancer.
         datePublished:2019-03-27T00:00:00Z
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            Cancer Research
            Biomedicine
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            Pathology
            Oncology
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      headline:ABT-263 exhibits apoptosis-inducing potential in oral cancer cells by targeting C/EBP-homologous protein
      description:ABT-263 is a potent BH3 mimetic that possesses anticancer potential against various types of cancer. In general, this potential is due to its high binding affinity to anti-apoptotic proteins in the Bcl-2 family that disrupt sequestration of pro-apoptotic proteins. In the present study, we sought to identify an alternative regulatory mechanism responsible for ABT-263-mediated anticancer activity in human oral cancer. We investigated the in vitro anti-cancer effects of ABT-263 using a trypan blue exclusion assay, Western blotting, DAPI staining, immunofluorescence staining, a live/dead assay, microarray-based expression profiling, and quantitative real-time PCR. In vivo anti-tumorigenic effects of ABT-263 were examined using a nude mouse tumor xenograft model, a TUNEL assay, and immunohistochemistry. We found that ABT-263 suppressed viability and induced apoptosis in human oral cancer-derived cell lines HSC-3 and HSC-4. Subsequent microarray-based gene expression profiling revealed 55 differentially expressed genes in the ABT-263-treatead group, including 12 genes associated with “endoplasmic reticulum stress and apoptosis.” Consistent with the microarray results, the mRNA expression levels of the top four genes (CHOP, TRB3, ASNS, and STC2) were found to be significantly increased. In addition, we found that ABT-263 considerably enhanced the expression levels of the C/EBP-homologous protein (CHOP) and its mRNA, resulting in apoptosis induction in four other human oral cancer-derived cell lines (MC-3, YD-15, HN22, and Ca9.22). Extending our in vitro findings, we found that ABT-263 reduced the growth of HSC-4 cells in vivo at a dosage of 100 mg/kg/day without any change in body weight. TUNEL-positive cells were also found to be increased in tumors of ABT-263-treated mice without any apparent histopathological changes in liver or kidney tissues. These results provide evidence that ABT-263 may serve as an effective therapeutic agent for the treatment of human oral cancer.
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         ABT-263
         Apoptosis
         CHOP
         ER stress
         Cancer Research
         Biomedicine
         general
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         Oncology
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