ArticlePloS one2013
Claudin-3 overexpression increases the malignant potential of colorectal cancer cells: roles of ERK1/2 and PI3K-Akt as modulators of EGFR signaling.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 61 citations in OpenAlex.
- Claudin proteins as emerging therapeutic targets for solid tumours.Nature reviews. Cancer · 2026Review
- Strain-specific protection of intestinal barrier by heat-treated plant-derived lactic acid bacteria via distinct tight junction modulation.Bioscience of microbiota, food and health · 2026Article
- The research trends and hotspots of claudins in the field of cancer.Cell adhesion & migration · 2025Review
- Synergistic Reduction of Breast Cancer Cell Viability and Aggressiveness Through Dual Inhibition of APE1 Redox Function and STAT3 Signaling.Cell biology international · 2025Article
- AOH induces oxidative stress and DNA damage in ovarian cancer cells via modulation of GPER1 and HIF1α/PI3K/CLDNs signaling pathway.Scientific reports · 2025Article
- PTEN Inactivation in Mouse Colonic Epithelial Cells Curtails DSS-Induced Colitis and Accelerates Recovery.Cancers · 2025Article
- MTCH2 promotes the malignant progression of ovarian cancer through the upregulation of AIMP2 expression levels, mitochondrial dysfunction and by mediating energy metabolism.Oncology letters · 2024Article
- The estrogen response in fibroblasts promotes ovarian metastases of gastric cancer.Nature communications · 2024Article
- Identification and validation of IRF6 related to ovarian cancer and biological function and prognostic value.Journal of ovarian research · 2024Article
- The Expression of the Claudin Family of Proteins in Colorectal Cancer.Biomolecules · 2024Review
- Expression patterns of claudins in cancer.Heliyon · 2023Review
- Interplay between EGFR, E-cadherin, and PTP1B in epidermal homeostasis.Tissue barriers · 2023Review
- Impairment of SK-MEL-28 Development-A Human Melanoma Cell Line-By theInternational journal of molecular sciences · 2023Article
- Claudin Barriers on the Brink: How Conflicting Tissue and Cellular Priorities Drive IBD Pathogenesis.International journal of molecular sciences · 2023Review
- PU.1-driven Th9 Cells Promote Colorectal Cancer in Experimental Colitis Models Through Il-6 Effects in Intestinal Epithelial Cells.Journal of Crohn's & colitis · 2022Article
- The role and mechanism of claudins in cancer.Frontiers in oncology · 2022Review
- Article
- Pre-exposure to hydrogen sulfide modulates the innate inflammatory response to organic dust.Cell and tissue research · 2021Article
- N‑glycosylation and receptor tyrosine kinase signaling affect claudin‑3 levels in colorectal cancer cells.Oncology reports · 2020Article
- Tight Junction Proteins and the Biology of Hepatobiliary Disease.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The altered expressions of claudin proteins have been reported during the tumorigenesis of colorectal cancer. However, the molecular mechanisms that regulate these events in this cancer type are poorly understood. Here, we report that epidermal growth factor (EGF) increases the expression of claudin-3 in human colorectal adenocarcinoma HT-29 cells. This increase was related to increased cell migration and the formation of anchorage-dependent and anchorage-independent colonies. We further showed that the ERK1/2 and PI3K-Akt pathways were involved in the regulation of these effects because specific pharmacological inhibition blocked these events. Genetic manipulation of claudin-1 and claudin-3 in HT-29 cells showed that the overexpression of claudin-1 resulted in decreased cell migration; however, migration was not altered in cells that overexpressed claudin-3. Furthermore, the overexpression of claudin-3, but not that of claudin-1, increased the tight junction-related paracellular flux of macromolecules. Additionally, an increased formation of anchorage-dependent and anchorage-independent colonies were observed in cells that overexpressed claudin-3, while no such changes were observed when claudin-1 was overexpressed. Finally, claudin-3 silencing alone despite induce increase proliferation, and the formation of anchoragedependent and -independent colonies, it was able to prevent the EGF-induced increased malignant potential. In conclusion, our results show a novel role for claudin-3 overexpression in promoting the malignant potential of colorectal cancer cells, which is potentially regulated by the EGF-activated ERK1/2 and PI3K-Akt pathways.
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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.