ArticleOncology reports2020
Sensitivity of allyl isothiocyanate to induce apoptosis via ER stress and the mitochondrial pathway upon ROS production in colorectal adenocarcinoma cells.
Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- The role of mitochondria-endoplasmic reticulum crosstalk in colorectal cancer.Genes & diseases · 2026Review
- The Role of Mitochondrial ROS in Neoplastic Transformations, Progression and Therapeutic Targeting.Oncology research · 2026Review
- Deciphering the interaction between the expression of LRP2 served as a mitochondrial metabolism-related gene and prognosis in colon cancer integrating multi-omics analysis.Discover oncology · 2025Article
- Health Benefits, Applications, and Analytical Methods of Freshly Produced Allyl Isothiocyanate.Foods (Basel, Switzerland) · 2025Review
- Molecular Subtypes based on Mitochondrial Oxidative Stress-related Gene Signature and Tumor Microenvironment Infiltration Characterization of Colon Adenocarcinoma.Current medicinal chemistry · 2025Article
- Characterization of mitochondrial metabolism related molecular subtypes and immune infiltration in colorectal adenocarcinoma.Scientific reports · 2024Article
- Review
- Chemopreventive aspects, investigational anticancer applications and current perspectives on allyl isothiocyanate (AITC): a review.Molecular and cellular biochemistry · 2023Review
- Allyl Isothiocianate Induces CaCells · 2023Article
- Nuclear endonuclease G controls cell proliferation in ovarian cancer.FEBS open bio · 2023Article
- From Natural Sources to Synthetic Derivatives: The Allyl Motif as a Powerful Tool for Fragment-Based Design in Cancer Treatment.Journal of medicinal chemistry · 2023Review
- Anticarcinogenic Effects of Isothiocyanates on Hepatocellular Carcinoma.International journal of molecular sciences · 2022Review
- Prognostic risk assessment model and drug sensitivity analysis of colon adenocarcinoma (COAD) based on immune-related lncRNA pairs.BMC bioinformatics · 2022Article
- Allyl-, Butyl- and Phenylethyl-Isothiocyanate Modulate Akt-mTOR and Cyclin-CDK Signaling in Gemcitabine- and Cisplatin-Resistant Bladder Cancer Cell Lines.International journal of molecular sciences · 2022Article
- Anticancer Activity, Mechanism, and Delivery of Allyl Isothiocyanate.Bioengineering (Basel, Switzerland) · 2022Review
- Allyl Isothiocyanate (AITC) Induces Apoptotic Cell Death In Vitro and Exhibits Anti-Tumor Activity in a Human Glioblastoma GBM8401/International journal of molecular sciences · 2022Article
- Bisimidazolium Salt Glycosyltransferase Inhibitors Suppress Hepatocellular Carcinoma Progression In Vitro and In Vivo.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Assessment of Methodological Pipelines for the Determination of Isothiocyanates Derived from Natural Sources.Antioxidants (Basel, Switzerland) · 2022Review
- Eradication of Myrosinase-Tethered Cancer Cells by Allyl Isothiocyanate Derived from Enzymatic Hydrolysis of Sinigrin.Pharmaceutics · 2022Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Allyl isothiocyanate (AITC), a bioactive phytochemical compound that is a constituent of dietary cruciferous vegetables, possesses promising chemopreventive and anticancer effects. However, reports of AITC exerting antitumor effects on apoptosis induction of colorectal cancer (CRC) cells in vitro are not well elucidated. The present study focused on the functional mechanism of the endoplasmic reticulum (ER) stress‑based apoptotic machinery induced by AITC in human colorectal cancer HT‑29 cells. Our results indicated that AITC decreased cell growth and number, reduced viability, and facilitated morphological changes of apoptotic cell death. DNA analysis by flow cytometry showed G2/M phase arrest, and alterations in the modulated protein levels caused by AITC were detected via western blot analysis. AITC also triggered vital intrinsic apoptotic factors (caspase‑9/caspase‑3 activity), disrupted mitochondrial membrane potential, and stimulated mitochondrial‑related apoptotic molecules (e.g., cytochrome c, apoptotic protease activating factor 1, apoptosis‑inducing factor, and endonuclease G). Additionally, AITC prompted induced cytosolic Ca2+ release and Ca2+‑dependent ER stress‑related signals, such as calpain 1, activating transcription factor 6α, glucose‑regulated proteins 78 and 94, growth arrest‑ and DNA damage‑inducible protein 153 (GADD153), and caspase‑4. The level of reactive oxygen species (ROS) production was found to induce the hallmark of ER stress GADD153, proapoptotic marker caspase‑3, and calpain activity after AITC treatment. Our findings showed for the first time that AITC induced G2/M phase arrest and apoptotic death via ROS‑based ER stress and the intrinsic pathway (mitochondrial‑dependent) in HT‑29 cells. Overall, AITC may exert an epigenetic effect and is a potential bioactive compound for CRC treatment.
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