ArticlePloS one2012
Inhibition of EGFR-AKT axis results in the suppression of ovarian tumors in vitro and in preclinical mouse model.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Association between dietary intake and risk of ovarian cancer: a systematic review and meta-analysis.European journal of nutrition · 2021Pooled it
- Structure-guided discovery and evaluation of an EGFR L858R-targeting peptide with antiproliferative activity against ovarian cancer cells.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Enhancing PARP inhibitor efficacy in ovarian cancer: targeting the PI3K/AKT/mTOR pathway.Journal of ovarian research · 2025Review
- Reviewing the Prospective Pharmacological Potential of Isothiocyanates in Fight against Female-Specific Cancers.Cancers · 2023Review
- Comparative transcriptomic analysis of gill reveals genes belonging to mTORC1 signaling pathway associated with the resistance trait of shrimp to VPFrontiers in immunology · 2023Article
- CTCFL regulates the PI3K-Akt pathway and it is a target for personalized ovarian cancer therapy.NPJ systems biology and applications · 2022Article
- Involvement of microRNA in Solid Cancer: Role and Regulatory Mechanisms.Biomedicines · 2021Review
- Role of Phytochemicals in Perturbation of Redox Homeostasis in Cancer.Antioxidants (Basel, Switzerland) · 2021Review
- Repurposing Pimavanserin, an Anti-Parkinson Drug for Pancreatic Cancer Therapy.Molecular therapy oncolytics · 2020Article
- Article
- Review
- ROS-Mediated Cancer Cell Killing through Dietary Phytochemicals.Oxidative medicine and cellular longevity · 2019Review
- Anti-Carcinogenic Glucosinolates in Cruciferous Vegetables and Their Antagonistic Effects on Prevention of Cancers.Molecules (Basel, Switzerland) · 2018Review
- BAG3 Protein Is Involved in Endothelial Cell Response to Phenethyl Isothiocyanate.Oxidative medicine and cellular longevity · 2018Article
- Inhibitory effect of the low-toxic exogenous aryl hydrocarbon receptor modulator 3'3-diindolylmethane on gastric cancer in mice.Oncology letters · 2017Article
- Phenethyl isothiocyanate suppresses the metastasis of ovarian cancer associated with the inhibition of CRM1-mediated nuclear export and mTOR-STAT3 pathway.Cancer biology & therapy · 2017Article
- Penfluridol: An Antipsychotic Agent Suppresses Metastatic Tumor Growth in Triple-Negative Breast Cancer by Inhibiting Integrin Signaling Axis.Cancer research · 2016Article
- PEITC treatment suppresses myeloid derived tumor suppressor cells to inhibit breast tumor growth.Oncoimmunology · 2015Article
- ROS Accumulation by PEITC Selectively Kills Ovarian Cancer Cells via UPR-Mediated Apoptosis.Frontiers in oncology · 2015Article
- Phenethyl isothiocyanate: a comprehensive review of anti-cancer mechanisms.Biochimica et biophysica acta · 2014Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Ovarian cancer is the leading cause of cancer related deaths in women. Genetic alterations including overexpression of EGFR play a crucial role in ovarian carcinogenesis. Here we evaluated the effect of phenethyl isothiocyanate (PEITC) in ovarian tumor cells in vitro and in vivo. Oral administration of 12 µmol PEITC resulted in drastically suppressing ovarian tumor growth in a preclinical mouse model. Our in vitro studies demonstrated that PEITC suppress the growth of SKOV-3, OVCAR-3 and TOV-21G human ovarian cancer cells by inducing apoptosis in a concentration-dependent manner. Growth inhibitory effects of PEITC were mediated by inhibition of EGFR and AKT, which are known to be overexpressed in ovarian tumors. PEITC treatment caused significant down regulation of constitutive protein levels as well as phosphorylation of EGFR at Tyr1068 in various ovarian cancer cells. In addition, PEITC treatment drastically reduced the phosphorylation of AKT which is downstream to EGFR and disrupted mTOR signaling. PEITC treatment also inhibited the kinase activity of AKT as observed by the down regulation of p-GSK in OVCAR-3 and TOV-21G cells. AKT overexpression or TGF treatment blocked PEITC induced apoptosis in ovarian cancer cells. These results suggest that PEITC targets EGFR/AKT pathway in our model. In conclusion, our study suggests that PEITC could be used alone or in combination with other therapeutic agents to treat ovarian cancer.
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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 OpenQuestion graph.