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http://scihub22266oqcxt.onion/ C5619256!5619256!28966729     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Cancer+Sci+Ther 2017 ; 9 (1): 298-306 Nephropedia Template TP {{tp|p=28966729|t=2017. Arsenic Trioxide Induces Apoptosis via Specific Signaling Pathways in HT-29 Colon Cancer Cells |pdf=|usr=}}{{28966729}} gab.com Text Arsenic Trioxide Induces Apoptosis via Specific Signaling Pathways in HT-29 Colon Cancer Cells JO: J Cancer Sci Ther http://www.kidney.de/pget.php?&tw=1&pmid=28966729 #FOAvip Background: Arsenic trioxide (ATO) is highly effective in the treatment of patients with acute promyelocytic leukemia (APL). It is a chemotherapeutic agent that has been shown to induce apoptosis in several tumor cell lines. However, research into its effects on colon carcinoma cells is still very limited. We previously reported that ATO is cytotoxic and causes DNA damage in HT-29 human colorectal adenocarcinoma cells. In the present study, we further evaluated its effect on oxidative stress (OS), and examined its apoptotic mechanisms of action on HT-29 cells. Methods: OS was assessed by spectrophotometric measurements of MDA levels while cell cycle analysis was evaluated by flow cytometry to determine whether ATO induces cell cycle arrest. Its effect on early apoptosis was also evaluated by flow cytometry using Annexin V-FITC/PI staining. Fluorescence microscopy was used to detect the morphological changes, and Western blotting was carried out to determine the expression of apoptosis-related proteins. Results: The lipid peroxidation assay revealed a dose-dependent increase in MDA production. DAPI staining showed morphological changes in the cell?s nucleus due to apoptosis. Cell cycle analysis and Annexin V-FITC assay also demonstrated a dose-dependent effect of ATO in the accumulation of cells at the sub G1 phase, and the percentages of Annexin V-positive cells, respectively. Western blot data showed that ATO upregulated the expression of caspase 3, Bax, and cytochrome C, and down-regulated the expression of Bcl-2. Conclusion: Taken together, our findings indicate that ATO induces OS and cytotoxicity in HT-29 cells through the mitochondria mediated intrinsic pathway of apoptosis. Twit Text FOAVip Arsenic Trioxide Induces Apoptosis via Specific Signaling Pathways in HT-29 Colon Cancer Cells ????J Cancer Sci Ther http://www.kidney.de/pget.php?&tw=1&pmid=28966729 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28966729 #FOAvip English Wikipedia <ref>{{Cite pmid|28966729}}</ref> Arsenic Trioxide Induces Apoptosis via Specific Signaling Pathways in HT-29 Colon Cancer Cells #MMPMID28966729 Stevens JJ; Graham B; Dugo E; Berhaneselassie-Sumner B; Ndebele K; Tchounwou PB J Cancer Sci Ther 2017[Jan]; 9 (1): 298-306 PMID28966729show ga Background: Arsenic trioxide (ATO) is highly effective in the treatment of patients with acute promyelocytic leukemia (APL). It is a chemotherapeutic agent that has been shown to induce apoptosis in several tumor cell lines. However, research into its effects on colon carcinoma cells is still very limited. We previously reported that ATO is cytotoxic and causes DNA damage in HT-29 human colorectal adenocarcinoma cells. In the present study, we further evaluated its effect on oxidative stress (OS), and examined its apoptotic mechanisms of action on HT-29 cells. Methods: OS was assessed by spectrophotometric measurements of MDA levels while cell cycle analysis was evaluated by flow cytometry to determine whether ATO induces cell cycle arrest. Its effect on early apoptosis was also evaluated by flow cytometry using Annexin V-FITC/PI staining. Fluorescence microscopy was used to detect the morphological changes, and Western blotting was carried out to determine the expression of apoptosis-related proteins. Results: The lipid peroxidation assay revealed a dose-dependent increase in MDA production. DAPI staining showed morphological changes in the cell?s nucleus due to apoptosis. Cell cycle analysis and Annexin V-FITC assay also demonstrated a dose-dependent effect of ATO in the accumulation of cells at the sub G1 phase, and the percentages of Annexin V-positive cells, respectively. Western blot data showed that ATO upregulated the expression of caspase 3, Bax, and cytochrome C, and down-regulated the expression of Bcl-2. Conclusion: Taken together, our findings indicate that ATO induces OS and cytotoxicity in HT-29 cells through the mitochondria mediated intrinsic pathway of apoptosis. äArsenic Trioxide Induces Apoptosis via Specific Signaling Pathways in (epmc).pdf DeepDyve Pubget Overpricing