alexa Arsenic Trioxide Induces Apoptosis via Specific Signaling Pathways in HT- 29 Colon Cancer Cells | OMICS International | Abstract
ISSN: 1948-5956

Journal of Cancer Science & Therapy
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Research Article

Arsenic Trioxide Induces Apoptosis via Specific Signaling Pathways in HT- 29 Colon Cancer Cells

Jacqueline J Stevens1*, Barbara Graham2, Erika Dugo1, Bezawit Berhaneselassie-Sumner1, Kenneth Ndebele2 and Paul B Tchounwou2*

1Molecular and Cellular Biology Research Laboratory, NIH RCMI-Center for Environmental Health, College of Science, Engineering and Technology, Jackson State University, Jackson, MS, USA

2Molecular Toxicology Research Laboratory, NIH RCMI-Center for Environmental Health, College of Science, Engineering and Technology, Jackson State University, Jackson, MS, USA

*Corresponding Author:
Jacqueline J Stevens
Molecular and Cellular Biology Research Laboratory
NIH RCMI-Center for Environmental Health, College of Science
Engineering and Technology, Jackson State University
1400 JR Lynch Street, Box 18540, Jackson, MS, USA
Tel: 6019795842
E-mail: [email protected]
Paul B Tchounwou
Molecular Toxicology Research Laboratory
NIH RCMI-Center for Environmental Health
College of Science, Engineering and Technology
Jackson State University, 1400 JR Lynch Street
Box 18540, Jackson, MS 39217, USA
Tel: 6019795842
E-mail: [email protected]

Received Date: September 07, 2016; Accepted Date: January 05, 2016; Published Date: January 09, 2016

Citation: Stevens JJ, Graham B, Dugo E, Berhaneselassie-Sumner B, Ndebele K, et al. (2016) Arsenic Trioxide Induces Apoptosis via Specific Signaling Pathways in HT-29 Colon Cancer Cells. J Cancer Sci Ther 9:298-306. doi: 10.4172/1948- 5956.1000432

Copyright: © 2016 Stevens JJ, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

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.

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