ArticleThe oncologist2012
Notch1-mediated tumor suppression in cervical cancer with the involvement of SST signaling and its application in enhanced SSTR-targeted therapeutics.
Article in The oncologist, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Notch signaling pathway in cancer: from mechanistic insights to targeted therapies.Signal transduction and targeted therapy · 2024Review
- Review
- Epigenetic regulation of somatostatin and somatostatin receptors in neuroendocrine tumors and other types of cancer.Reviews in endocrine & metabolic disorders · 2021Review
- Relevance research between the expression of p16Journal of clinical laboratory analysis · 2020Article
- Genes Regulated by HPV 16 E6 and High Expression of NFX1-123 in Cervical Cancers.OncoTargets and therapy · 2020Article
- Regulation of somatostatin expression by vitamin D3 and valproic acid in human adipose-derived mesenchymal stem cells.Stem cell research & therapy · 2019Article
- DAPT, a γ-Secretase Inhibitor, Suppresses Tumorigenesis, and Progression of Growth Hormone-Producing Adenomas by Targeting Notch Signaling.Frontiers in oncology · 2019Article
- HDAC inhibitors suppressed small cell lung cancer cell growth and enhanced the suppressive effects of receptor-targeting cytotoxins via upregulating somatostatin receptor II.American journal of translational research · 2018Article
- Gene Expression Analysis Identifies Novel Targets for Cervical Cancer Therapy.Frontiers in immunology · 2018Article
- Dihydromyricetin-mediated inhibition of the Notch1 pathway induces apoptosis in QGY7701 and HepG2 hepatoma cells.World journal of gastroenterology · 2017Article
- Zeylenone, a naturally occurring cyclohexene oxide, inhibits proliferation and induces apoptosis in cervical carcinoma cells via PI3K/AKT/mTOR and MAPK/ERK pathways.Scientific reports · 2017Article
- Notch is a critical regulator in cervical cancer by regulating Numb splicing.Oncology letters · 2017Article
- Article
- Notch Signaling Activation in Cervical Cancer Cells Induces Cell Growth Arrest with the Involvement of the Nuclear Receptor NR4A2.Journal of Cancer · 2016Article
- Cervical cancer stem cells.Cell proliferation · 2015Review
- The Histone Deacetylase Inhibitor Vaproic Acid Induces Cell Growth Arrest in Hepatocellular Carcinoma Cells via Suppressing Notch Signaling.Journal of Cancer · 2015Article
- Emerging biological treatments for uterine cervical carcinoma.Journal of Cancer · 2014Review
- The notch ligand JAGGED1 as a target for anti-tumor therapy.Frontiers in oncology · 2014Review
- The challenge of targeting notch in hematologic malignancies.Frontiers in pediatrics · 2014Review
- Role of Notch signalling pathway in cancer and its association with DNA methylation.Journal of genetics · 2013Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
The role of Notch signaling in cervical cancer is seemingly controversial. To confirm the function of Notch signaling in this type of cancer, we established a stable Notch1-activated cervical cancer HeLa cell line. We found that Notch1 activation resulted in apoptosis, cell cycle arrest, and tumor suppression. At the molecular level, we found that a variety of genes associated with cyclic AMP, G protein-coupled receptor, and cancer signaling pathways contributed to Notch1-mediated tumor suppression. We observed that the expression of somatostatin (SST) was dramatically induced by Notch1 signaling activation, which was accompanied by enhanced expression of the cognate SST receptor subtype 1 (SSTR1) and SSTR2. Certain genes, such as tumor protein 63 (TP63, p63), were upregulated, whereas others, such as B-cell lymphoma 2 (BCL-2), Myc, Akt, and STAT3, were downregulated. Subsequently, knockdown of Notch1-induced SST reversed Notch1-induced decrease of BCL-2 and increase of p63, indicating that Notch1-induced tumor suppression may be partly through upregulating SST signaling. Our findings support a possible crosstalk between Notch signaling and SST signaling. Moreover, Notch-induced SSTR activation could enhance SSTR-targeted cancer chemotherapy. Valproic acid (VPA), a histone deacetylase inhibitor, suppressed cell growth and upregulated the expression of Notch1 and SSTR2. A combination therapy with VPA and the SSTR2-targeting cytotoxic conjugate CPT-SST strongly led to greater suppression, as compared to each alone. Our findings thus provide us with a promising clinical opportunity for enhanced cancer therapy using combinations of Notch1-activating agents and SSTR2-targeting agents.
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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.