ArticleBMC cancer2018
Gap junctions contribute to anchorage-independent clustering of breast cancer cells.
Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Noninvasive real-time monitoring of cellular spatiotemporal dynamics via machine learning-enhanced electrical impedance spectroscopy.Science advances · 2025Article
- Pseudorabies virus infection triggers pUL46-mediated phosphorylation of connexin-43 and closure of gap junctions to promote intercellular virus spread.PLoS pathogens · 2025Article
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- Harnessing immunotherapy for brain metastases: insights into tumor-brain microenvironment interactions and emerging treatment modalities.Journal of hematology & oncology · 2023Review
- Cell Adhesion Molecules Affected by Ionizing Radiation and Estrogen in an Experimental Breast Cancer Model.International journal of molecular sciences · 2022Article
- HMMR promotes peritoneal implantation of gastric cancer by increasing cell-cell interactions.Discover oncology · 2022Article
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- Collective metastasis: coordinating the multicellular voyage.Clinical & experimental metastasis · 2021Review
- Using dynamic cell communication improves treatment strategies of breast cancer.Cancer cell international · 2021Review
- Mitotic arrest affects clustering of tumor cells.Cell division · 2021Article
- Flow-regulated endothelial glycocalyx determines metastatic cancer cell activity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- GJA1 is a Prognostic Biomarker and Correlated with Immune Infiltrates in Colorectal Cancer.Cancer management and research · 2020Article
- Article
- Article
- Emerging roles of gap junction proteins connexins in cancer metastasis, chemoresistance and clinical application.Journal of biomedical science · 2019Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCancer cell aggregation is a key process involved in the formation of clusters of circulating tumor cells. We previously reported that cell-cell adhesion proteins, such as E-cadherin, and desmosomal proteins are involved in cell aggregation to form clusters independently of cell migration or matrix adhesion. Here, we investigated the involvement of gap junction intercellular communication (GJIC) during anchorage-independent clustering of MCF7 breast adenocarcinoma cells.
methodsWe used live cell image acquisition and analysis to monitor the kinetics of MCF7 cell clustering in the presence/absence of GJIC pharmacological inhibitors and to screen a LOPAC® bioactive compound library. We also used a calcein transfer assay and flow cytometry to evaluate GJIC involvement in cancer cell clustering.
resultsWe first demonstrated that functional GJIC are established in the early phase of cancer cell aggregation. We then showed that pharmacological inhibition of GJIC using tonabersat and meclofenamate delayed MCF7 cell clustering and reduced calcein transfer. We also found that brefeldin A, an inhibitor of vesicular trafficking, which we identified by screening a small compound library, and latrunculin A, an actin cytoskeleton-disrupting agent, both impaired MCF7 cell clustering and calcein transfer.
conclusionsOur results demonstrate that GJIC are involved from the earliest stages of anchorage-independent cancer cell aggregation. They also give insights into the regulatory mechanisms that could modulate the formation of clusters of circulating tumor 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.