ArticleJournal of translational medicine2019
Role of MAML1 in targeted therapy against the esophageal cancer stem cells.
Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 44 citations in OpenAlex.
- MAML1 drives Notch and Hedgehog oncogenic pathways by inhibiting Itch activity in triple-negative breast cancer.Cell death and differentiation · 2026Article
- The dual role of the Notch signaling pathway in digestive system cancers.European journal of medical research · 2026Review
- Targeting notch signaling pathway in esophageal cancer: from molecular insights to therapies.Oncology reviews · 2026Review
- Signaling pathways as the pivotal regulators of cisplatin resistance in tumor cells through SOX2 upregulation.Medical oncology (Northwood, London, England) · 2025Review
- β-catenin as a key regulator of the cisplatin response in tumor cells.Clinical and experimental medicine · 2025Review
- Role ofMolecular biology research communications · 2025Article
- 4,5-Dimethoxycanthin-6-one Inhibits Glioblastoma Stem Cell and Tumor Growth by Inhibiting TSPAN1 Interaction with TM4SF1.Neurochemical research · 2024Article
- CD44 and its implication in neoplastic diseases.MedComm · 2024Review
- PI3K/AKT pathway as a pivotal regulator of epithelial-mesenchymal transition in lung tumor cells.Cancer cell international · 2024Review
- MicroRNA-495: a therapeutic and diagnostic tumor marker.Journal of molecular histology · 2023Review
- PI3K/AKT signaling pathway as a critical regulator of epithelial-mesenchymal transition in colorectal tumor cells.Cell communication and signaling : CCS · 2023Review
- Role of microRNAs in regulation of doxorubicin and paclitaxel responses in lung tumor cells.Cell division · 2023Review
- MicroRNA-506 as a tumor suppressor in anaplastic thyroid carcinoma by regulation of WNT and NOTCH signaling pathways.Iranian journal of basic medical sciences · 2023Article
- LINC00667 Promotes Progression of Esophageal Cancer Cells by Regulating miR-200b-3p/SLC2A3 Axis.Digestive diseases and sciences · 2022Article
- MicroRNAs as the critical regulators of cell migration and invasion in thyroid cancer.Biomarker research · 2022Review
- Long non-coding RNAs as the critical regulators of epithelial mesenchymal transition in colorectal tumor cells: an overview.Cancer cell international · 2022Review
- Gynecologic Cancer, Cancer Stem Cells, and Possible Targeted Therapies.Frontiers in pharmacology · 2022Review
- MicroRNAs as the critical regulators of Cisplatin resistance in ovarian cancer cells.Journal of ovarian research · 2021Review
- Molecular mechanisms of the microRNA-132 during tumor progressions.Cancer cell international · 2021Review
- Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEsophageal cancer is the sixth-leading cause of cancer-related deaths worldwide. Cancer stem cells (CSCs) are the main reason for tumor relapse in esophageal squamous cell carcinoma (ESCC). The NOTCH pathway is important in preservation of CSCs, therefore it is possible to target such cells by targeting MAML1 as the main component of the NOTCH transcription machinery.
methodsIn present study we isolated the CD44+ ESCC CSCs and designed a MAML1-targeted therapy to inhibit the NOTCH signaling pathway. CSCs were isolated using magnetic cell sorting utilizing the CD44 cell surface marker. Several stem cell markers were analyzed in the levels of protein and mRNA expression. The isolated CSCs were characterized in vivo in NUDE mice. Biological role of MAML1 was assessed in isolated CD44+ CSCs. A drug resistance assay was also performed to assess the role of MAML1 in CD44+ CSCs with 5FU resistance.
resultsThe CD44+ CSCs had ability to form tumors in NUDE mice. MAML1 silencing caused a significant decrease (p = 0.019) and ectopic expression caused a significant increase in migration of CD44+ CSCs (p = 0.012). Moreover, MAML1 silencing and ectopic expression significantly increased and decreased 5FU resistance, respectively (p < 0.05). MAML1 silencing significantly increased the number of cells in G1 phase (p = 0.008), and its ectopic expression significantly increased the number of CD44+ CSCS in S phase (p = 0.037).
conclusionsMAML1 may be utilized for targeted therapy with a low side effect to eliminate the CD44+ CSCs through inhibition of canonical NOTCH pathway in ESCC patients.
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