ArticleScientific reports2017
Benzyl Isothiocyanate potentiates p53 signaling and antitumor effects against breast cancer through activation of p53-LKB1 and p73-LKB1 axes.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- Bio-functional and anti-cancer (MCF-7) benzyl isothiocyanate nanoemulsions preparation using green pressurized water and process optimization.Scientific reports · 2026Article
- Spermine Oxidase Serves as a Key Functional Node in Microbial Dysbiosis-Induced Breast Carcinogenesis.Cancer research · 2026Article
- Notch-1 suppressed vascular dementia via modulating AMPK/mTOR/TFEB/YAP signaling induced ferroptosis.European journal of medical research · 2026Article
- A pro-carcinogenic oral microbe internalized by breast cancer cells promotes mammary tumorigenesis.Cell communication and signaling : CCS · 2026Article
- Synergistic targeting of cancer-related proteins by benzyl isothiocyanate and caffeic acid: MLSD and cytotoxic mechanisms in MCF-7 cells.3 Biotech · 2025Article
- New Contributions to Deepen the Quality-Based Safety Assessment in the Consumption of Edible Nasturtium Flowers-The Role of Volatilome.Life (Basel, Switzerland) · 2025Article
- Benzyl isothiocyanate suppresses development of thyroid carcinoma by regulating both autophagy and apoptosis pathway.iScience · 2024Article
- Reviewing the Prospective Pharmacological Potential of Isothiocyanates in Fight against Female-Specific Cancers.Cancers · 2023Review
- Chemical Composition and Biological Activity of Essential Oil and Extract from the Seeds ofFood technology and biotechnology · 2022Article
- Review
- Hydrogen Sulfide Biology and Its Role in Cancer.Molecules (Basel, Switzerland) · 2022Review
- Inverse molecular docking reveals a novel function of thymol: Inhibition of fat deposition induced by high-dose glucose inFood science & nutrition · 2021Article
- Estrogen Receptor-Alpha and p53 Status as Regulators of AMPK and mTOR in Luminal Breast Cancer.Cancers · 2021Article
- The Cross Talk Between p53 and mTOR Pathways in Response to Physiological and Genotoxic Stresses.Frontiers in cell and developmental biology · 2021Review
- MicroRNA-1246 by Targeting AXIN2 and GSK-3β Overcomes Drug Resistance and Induces Apoptosis in Chemo-resistant Leukemia Cells.Journal of Cancer · 2021Article
- OncoOmics approaches to reveal essential genes in breast cancer: a panoramic view from pathogenesis to precision medicine.Scientific reports · 2020Article
- The Diverse Functions of Mutant 53, Its Family Members and Isoforms in Cancer.International journal of molecular sciences · 2019Review
- Bioactive Compounds: Multi-Targeting Silver Bullets for Preventing and Treating Breast Cancer.Cancers · 2019Review
- Role of Phytochemicals in Cancer Prevention.International journal of molecular sciences · 2019Review
- Benzyl isothiocyanate suppresses development and metastasis of murine mammary carcinoma by regulating the Wnt/β‑catenin pathway.Molecular medicine reports · 2019Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Functional reactivation of p53 pathway, although arduous, can potentially provide a broad-based strategy for cancer therapy owing to frequent p53 inactivation in human cancer. Using a phosphoprotein-screening array, we found that Benzyl Isothiocynate, (BITC) increases p53 phosphorylation in breast cancer cells and reveal an important role of ERK and PRAS40/MDM2 in BITC-mediated p53 activation. We show that BITC rescues and activates p53-signaling network and inhibits growth of p53-mutant cells. Mechanistically, BITC induces p73 expression in p53-mutant cells, disrupts the interaction of p73 and mutant-p53, thereby releasing p73 from sequestration and allowing it to be transcriptionally active. Furthermore, BITC-induced p53 and p73 axes converge on tumor-suppressor LKB1 which is transcriptionally upregulated by p53 and p73 in p53-wild-type and p53-mutant cells respectively; and in a feed-forward mechanism, LKB1 tethers with p53 and p73 to get recruited to p53-responsive promoters. Analyses of BITC-treated xenografts using LKB1-null cells corroborate in vitro mechanistic findings and establish LKB1 as the key node whereby BITC potentiates as well as rescues p53-pathway in p53-wild-type as well as p53-mutant cells. These data provide first in vitro and in vivo evidence of the integral role of previously unrecognized crosstalk between BITC, p53/LKB1 and p73/LKB1 axes in breast tumor growth-inhibition.
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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 Socratic graph.