ArticleCancer biology & therapy2018
Blocking NOTCH pathway can enhance the effect of EGFR inhibitor through targeting CD133+ endometrial cancer cells.
Article in Cancer biology & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Natural Products in Endometrial Cancer: Molecular Mechanisms, Preclinical Evidence, and Clinical Perspectives.Current issues in molecular biology · 2026Review
- Fueling the Seed: Growth Factors and Cytokines Driving Cancer Stem Cells in Gynecological Malignancies.International journal of molecular sciences · 2025Review
- PAX2 induces endometrial cancer by inhibiting mitochondrial function via the CD133-AKT1 pathway.Molecular and cellular biochemistry · 2025Article
- Identification of increased dedifferentiation along the Prom1+ cancer cells in Müllerian adenosarcoma with sarcomatous overgrowth.British journal of cancer · 2025Article
- Study Deciphering the Crucial Involvement of Notch Signaling Pathway in Human Cancers.Endocrine, metabolic & immune disorders drug targets · 2024Review
- Can CD133 Be Regarded as a Prognostic Biomarker in Oncology: Pros and Cons.International journal of molecular sciences · 2023Review
- New insights for gynecological cancer therapies: from molecular mechanisms and clinical evidence to future directions.Cancer metastasis reviews · 2023Review
- Endometrial Cancer Stem Cells: Where Do We Stand and Where Should We Go?International journal of molecular sciences · 2022Review
- Bone Marrow-Derived Cells in Endometrial Cancer Pathogenesis: Insights from Breast Cancer.Cells · 2022Review
- Components ofJournal of oncology · 2022Article
- ZIC2 upregulates lncRNA SNHG12 expression to promote endometrial cancer cell proliferation and migration by activating the Notch signaling pathway.Molecular medicine reports · 2021Article
- B3GNT3 acts as a carcinogenic factor in endometrial cancer via facilitating cell growth, invasion and migration through regulating RhoA/RAC1 pathway-associated markers.Genes & genomics · 2021Article
- Notch signaling in female cancers: a multifaceted node to overcome drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2021Review
- Targeted therapies in gynecological cancers: a comprehensive review of clinical evidence.Signal transduction and targeted therapy · 2020Review
- Expression Profiles of the Phosphatase and Tensin Homolog (PTEN), CDH1, and CDH2 Genes, and the Cell Membrane Protein, CD133, in the Ishikawa Human Endometrial Adenocarcinoma Cell Line.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Review
- Knockdown of long non-coding RNA SNHG5 inhibits malignant cellular phenotypes of glioma via Wnt/CTNNB1 signaling pathway.Journal of Cancer · 2019Article
- Long Non-coding RNA CDKN2B Antisense RNA 1 Gene Contributes to Paclitaxel Resistance in Endometrial Carcinoma.Frontiers in oncology · 2019Article
- Transit-Amplifying Cells in the Fast Lane from Stem Cells towards Differentiation.Stem cells international · 2017Review
- Expression of CD133 in endometrial cancer cells and its implications.Journal of Cancer · 2017Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the molecular therapeutics targeting key biomarkers such as epithelial growth factor receptor (EGFR), PI3K/AKT/mTOR, and vascular endothelial growth factor (VEGF) shows some success in clinical trials, some internally existing challenges in endothelial cancer biology hinder the drug effects. One of the major challenges stems from cancer stem cell-derived drug resistance. CD133 positive cells are well believed as cancer stem cells (CSC) in endometrial cancers and NOTCH pathway plays a critical role in retaining CD133+ cells by promoting CSC self-renewal and chemoresistance. Here, we initiated a therapeutic strategy to improve effects of EGFR inhibition by targeting NOTCH pathway of CD133+ cells in endometrial cancers. We first detected and purified the CD133+ cell fraction in endometrial cancer cell line Ishikawa (IK), and validated activation of NOTCH pathway in the CD133+ cells that have higher proliferation rate and lower apoptosis rate, comparing to CD133- cells. Results of nude mouse xenograft experiments further demonstrated CD133+ cells retain higher tumorigenesis capacity than CD133- cells, indicating their tumor-initiating property. Last, we applied both NOTCH inhibitor DAPT and EGFR inhibitor AG1478 treatment on endometrial cancer lines IK and HEC-1A and the results suggested improvement effects of the combination therapy compared to the treatments of DAPT or AG1478 alone. These findings indicated targeting NOTCH pathway in CD133+ cells, combining with EGFR inhibition, which provides a novel therapeutic strategy for endometrial cancer diseases.
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