ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Cervical Cancer Cell Growth, Drug Resistance, and Epithelial-Mesenchymal Transition Are Suppressed by y-Secretase Inhibitor RO4929097.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Artemisinin Inhibits Drug Resistance and Epithelial-Mesenchymal Transition in Cervical Cancer Cells via the Wnt/β-Catenin Signaling Pathway.Bulletin of experimental biology and medicine · 2025Article
- Integrative bioinformatics and experimental validation unveil CRISP3 as a hypoxia-, epithelial mesenchymal transition-, and immune-related prognostic biomarker and therapeutic target in breast cancer.Frontiers in immunology · 2025Article
- Anticancer Potential of Valencia Peanut (Foods (Basel, Switzerland) · 2024Article
- The non-apoptotic function of Caspase-8 in negatively regulating the CDK9-mediated Ser2 phosphorylation of RNA polymerase II in cervical cancer.Cellular and molecular life sciences : CMLS · 2022Article
- Simple and automatic monitoring of cancer cell invasion into an epithelial monolayer using label-free holographic microscopy.Scientific reports · 2022Article
- A Novel Dialkylamino-Functionalized Chalcone, DML6, Inhibits Cervical Cancer Cell Proliferation, In Vitro, via Induction of Oxidative Stress, Intrinsic Apoptosis and Mitotic Catastrophe.Molecules (Basel, Switzerland) · 2021Article
- MicroRNA-143 Sensitizes Cervical Cancer Cells to Cisplatin: a Promising Anticancer Combination Therapy.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Impact of Poly (Styrene-Acrylic Acid) Latex Nanoparticles on Colorectal and Cervical Cancer Cells.Polymers · 2021Article
- Notch signaling in female cancers: a multifaceted node to overcome drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2021Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The Notch signaling pathway has been reported to play a pivotal role in tumorigenesis. Emerging evidence has demonstrated that the Notch signaling pathway regulates several cellular processes. The present study investigated the effect of the Notch signaling pathway on cell growth, invasiveness, and drug resistance, as well as epithelial-mesenchymal transition (EMT), of cervical cancer cells. MATERIAL AND METHODS We used quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analysis to measure the expression level of Notch2. CCK-8, clonality, wound healing, and Transwell assays were used to evaluate the effect of γ-secretase inhibitor (GSI) RO4929097 on cervical cancer cell lines HeLa and Caski. To explore the role of the Notch signaling pathway in EMT, the epithelial and mesenchymal markers were detected by qRT-PCR and Western blot after cervical cancer cell lines were treated with GSI RO4929097. RESULTS The expression of Notch2 was found to increase in cervical cancer cell lines compared with the normal immortalized human cervical epithelial cells. GSI RO4929097 was confirmed to inhibit the Notch signaling pathway and impaired the proliferation, drug resistance, migration, and invasion abilities of cervical cancer cells. The protein expression levels of the mesenchymal biomarkers Snail, Twist, and neural cadherin (N-cadherin) decreased; however, the expression of the epithelial biomarker epithelial cadherin (E-cadherin) increased in the cervical cancer cells treated with GSI RO4929097. CONCLUSIONS Notch signaling pathway plays an important role in the development and progression of cervical cancer. Blockade of the Notch pathway using GSI RO4929097 inhibited cell growth and reduced chemoresistance, invasion, metastasis, and EMT in cervical cancer cells.
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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.