ArticleNutrition and cancer2014
Phenethyl isothiocyanate inhibits proliferation and induces apoptosis in pancreatic cancer cells in vitro and in a MIAPaca2 xenograft animal model.
Article in Nutrition and cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 32 citations in OpenAlex.
- Cruciferous vegetable consumption and the risk of pancreatic cancer: a meta-analysis.World journal of surgical oncology · 2015Pooled it
- PEITC in End-Stage B-Cell Prolymphocytic Leukemia: Case Report of Possible Sensitization to Salvage R-CHOP.The Permanente journalPooled it
- Unlocking the Potential of Bioactive Compounds in Pancreatic Cancer Therapy: A Promising Frontier.Biomolecules · 2025Review
- Notch signaling pathway modulation by food functional ingredients: mechanisms, cancer and immunoregulation.Frontiers in cell and developmental biology · 2025Review
- Brassicaceae Mustards: Phytochemical Constituents, Pharmacological Effects, and Mechanisms of Action against Human Disease.International journal of molecular sciences · 2024Review
- Review
- Diallyl Trisulfide Induces Apoptosis in Breast Ductal Carcinoma In Situ Derived and Minimally Invasive Breast Cancer Cells.Nutrients · 2022Article
- Modulation of Notch Signaling Pathway by Bioactive Dietary Agents.International journal of molecular sciences · 2022Review
- Targeting Histone Deacetylases: Opportunities for Cancer Treatment and Chemoprevention.Pharmaceutics · 2022Review
- New possible silver lining for pancreatic cancer therapy: Hydrogen sulfide and its donors.Acta pharmaceutica Sinica. B · 2021Review
- Article
- The Role of Isothiocyanates as Cancer Chemo-Preventive, Chemo-Therapeutic and Anti-Melanoma Agents.Antioxidants (Basel, Switzerland) · 2019Review
- Dietary phytochemical PEITC restricts tumor development via modulation of epigenetic writers and erasers.Scientific reports · 2017Article
- Histone and Non-Histone Targets of Dietary Deacetylase Inhibitors.Current topics in medicinal chemistry · 2016Review
- Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition.Seminars in cancer biology · 2015Review
- Phenethyl isothiocyanate: a comprehensive review of anti-cancer mechanisms.Biochimica et biophysica acta · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Pancreatic cancer is often diagnosed at an advanced stage and it has a poor prognosis that points to an increased need to develop effective chemoprevention strategies for this disease. We examined the ability of phenethyl isothiocyanate (PEITC), a naturally occurring isothiocyanate found in cruciferous vegetables, to inhibit the growth of pancreatic cancer cells in vitro and in a MIAPaca2 xenograft animal model. Exposure to PEITC inhibited pancreatic cancer cell growth in a dose-dependent manner, with an IC50 of approximately 7 μmol/L. PEITC treatment induced G2/M phase cell cycle arrest, downregulated the antiapoptotic proteins Bcl-2 and Bcl-XL, upregulated the proapoptotic protein Bak, and suppressed Notch 1 and 2 levels. In addition, treatment with PEITC induced cleavage of poly-(ADP-ribose) polymerase and led to increased cytoplasmic histone-associated DNA fragmentation and subdiploid (apoptotic) fraction in pancreatic cancer cells. Oral administration of PEITC suppressed the growth of pancreatic cancer cells in a MIAPaca2 xenograft animal model. Our data show that PEITC exerts its inhibitory effect on pancreatic cancer cells through several mechanisms, including G2/M phase cell cycle arrest and induction of apoptosis, and supports further investigation of PEITC as a chemopreventive agent for pancreatic cancer.
Indexed as
Identifiers
What 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.