ArticleInternational journal of molecular sciences2018
Caffeic Acid and Metformin Inhibit Invasive Phenotype Induced by TGF-β1 in C-4I and HTB-35/SiHa Human Cervical Squamous Carcinoma Cells by Acting on Different Molecular Targets.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Precision theranostics in cervical Cancer: Harnessing stimuli-responsive hydrogels for tumor microenvironment-targeted therapy and diagnosis.Materials today. Bio · 2025Review
- Anti-metastasis activity of 5,4'-dihydroxy 6,8-dimethoxy 7-O-rhamnosyl flavone from Indigofera aspalathoides Vahl on breast cancer cells.Scientific reports · 2024Article
- Impact of AMPK on cervical carcinoma progression and metastasis.Cell death & disease · 2023Article
- Anticancer Effect of Pomegranate Peel Polyphenols against Cervical Cancer.Antioxidants (Basel, Switzerland) · 2023Review
- Caffeic Acid and Diseases-Mechanisms of Action.International journal of molecular sciences · 2022Review
- Article
- Infection by High-Risk Human Papillomaviruses, Epithelial-to-Mesenchymal Transition and Squamous Pre-Malignant or Malignant Lesions of the Uterine Cervix: A Series of Chained Events?International journal of molecular sciences · 2021Review
- Metformin Potentiates the Anticancer Effect of Everolimus on Cervical Cancer In Vitro and In Vivo.Cancers · 2021Article
- Review
- Selective Cytotoxicity of Complexes with N,N,N-Donor Dipodal Ligand in Tumor Cells.International journal of molecular sciences · 2021Article
- Caffeic Acid Supplement Alleviates Colonic Inflammation and Oxidative Stress Potentially Through Improved Gut Microbiota Community in Mice.Frontiers in microbiology · 2021Article
- Metformin induces apoptosis and inhibits migration by activating the AMPK/p53 axis and suppressing PI3K/AKT signaling in human cervical cancer cells.Molecular medicine reports · 2021Article
- Metformin Downregulates PD-L1 Expression in Esophageal Squamous Cell Catrcinoma by Inhibiting IL-6 Signaling Pathway.Frontiers in oncology · 2021Article
- Review
- Vimentin as a target for the treatment of COVID-19.BMJ open respiratory research · 2020Article
- Animals in Iodine Deficiency or Sulfadimethoxine Models of Thyroid Damage Are Differently Affected by the Consumption of Brassica Sprouts.Biological trace element research · 2020Article
- Mechanisms of metformin inhibiting cancer invasion and migration.American journal of translational research · 2020Review
- Article
- Article
- Restoring E-cadherin Expression by Natural Compounds for Anticancer Therapies in Genital and Urinary Cancers.Molecular therapy oncolytics · 2019Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the progression of epithelial cancer, the cells may lose epithelial markers and gain mesenchymal phenotype via Epithelial-Mesenchymal Transition (EMT). Such transformation of epithelial cancer cells to mesenchymal-like characteristic benefits plasticity and supports their ability to migrate. The aim of this study was to evaluate the influence of natural compound Caffeic Acid (CA) alone and in combination with antidiabetic drug Metformin (Met) on metastatic progression of two human cervical squamous cell cancer lines, C-4I and HTB-35/SiHa cells. EMT program was triggered by exposition of both epithelial cell lines to TGF-β1. Gene expression patterns related to epithelial/mesenchymal phenotype were evaluated by Real-Time PCR analysis and the protein amount was detected by western blot. The treatment of human squamous cancer cells with CA and with Met, suppressed the motility of cells and the effect depended on a particular cell line. Both compounds regulated the EMT process in C4-I and HTB-35 cells by interfering with different molecular targets. In TGF-β1-stimulated C4-I cells, CA suppressed the expression of mesenchymal transcription factor SNAI1 which resulted in enhanced expression of epithelial markers E-cadherin, Occludin and Claudin. Additionally, CA blocked
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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.