ArticleJournal of cancer science & therapy2017
Arsenic Trioxide Induces Apoptosis via Specific Signaling Pathways in HT-29 Colon Cancer Cells.
Article in Journal of cancer science & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The trial behind it
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Perindopril and L‑arginine protect against arsenic trioxide-induced neurotoxicity via Keap1/Nrf2/HO‑1 activation and suppression of neuroinflammation and apoptosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Arsenic Trioxide and the MNK1 Inhibitor AUM001 Exert Synergistic Anti-Glioblastoma Effects by Modulating Key Translational, Cell Cycle, and Transmembrane Transport Pathways.Brain sciences · 2026Article
- Arsenic enhances cervical cancer cell radiosensitivity by suppressing the DNA damage repair pathway.Translational cancer research · 2025Article
- Asciminib, a novel allosteric inhibitor of BCR-ABL1, shows synergistic effects when used in combination with imatinib with or without drug resistance.Pharmacology research & perspectives · 2024Article
- Article
- Arsenic Trioxide Decreases Lymphangiogenesis by Inducing Apoptotic Pathways and Inhibition of Important Endothelial Cell Receptors.Current issues in molecular biology · 2023Article
- Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria.International journal of molecular sciences · 2023Review
- Organoiridium Complexes Enhance Cellular Defense Against Reactive Aldehydes Species.Chemistry (Weinheim an der Bergstrasse, Germany) · 2023Article
- Promising Strategy of mPTP Modulation in Cancer Therapy: An Emerging Progress and Future Insight.International journal of molecular sciences · 2023Review
- Targeting Cell Death Mechanism Specifically in Triple Negative Breast Cancer Cell Lines.International journal of molecular sciences · 2022Article
- Down-regulation of RdRp complex and activated immune response due to increased arsenic level leads to decreased corona virus replication.Current research in microbial sciences · 2022Article
- Circ_0031242 Silencing Mitigates the Progression and Drug Resistance in DDP-Resistant Hepatoma Cells by the miR-924/POU3F2 Axis.Cancer management and research · 2021Article
- Article
- Targeting the Mitochondrial Metabolic Network: A Promising Strategy in Cancer Treatment.International journal of molecular sciences · 2020Review
- Erythrocyte Membrane-Coated Arsenic Trioxide-Loaded Sodium Alginate Nanoparticles for Tumor Therapy.Pharmaceutics · 2019Article
- Downregulation ofFuture science OA · 2019Article
- Hepatic Arterial Chemoembolization With Arsenic Trioxide Eluting CalliSpheres Microspheres Versus Lipiodol Emulsion: Pharmacokinetics And Intratumoral Concentration In A Rabbit Liver Tumor Model.Cancer management and research · 2019Article
- Interplay between NRF1, E2F4 and MYC transcription factors regulating common target genes contributes to cancer development and progression.Cellular oncology (Dordrecht, Netherlands) · 2018Review
- PI3K/Akt/mTOR Signaling Pathway and the Biphasic Effect of Arsenic in Carcinogenesis.Molecular pharmacology · 2018Review
- Preparation and characterization of erythrocyte membrane cloaked PLGA/arsenic trioxide nanoparticles and evaluation of theirRSC advances · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundArsenic 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.
methodsOS 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.
resultsThe 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.
conclusionTaken together, our findings indicate that ATO induces OS and cytotoxicity in HT-29 cells through the mitochondria mediated intrinsic pathway of apoptosis.
Indexed as
Identifiers
28966729PMC5619256W2588785745What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.