ArticleClinical & experimental metastasis2012
The gap junction protein Cx43 is involved in the bone-targeted metastatic behaviour of human prostate cancer cells.
Article in Clinical & experimental metastasis, 2012. 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, 56 citations in OpenAlex.
- Review
- Lack of canonical activities of connexins in highly aggressive human prostate cancer cells.Biological research · 2024Article
- Review
- Hypersensitive intercellular responses of endometrial stromal cells drive invasion in endometriosis.eLife · 2024Article
- Integrative analyses identified gap junction beta-2 as a prognostic biomarker and therapeutic target for breast cancer.Cancer innovation · 2024Article
- Comprehensive Pan-Cancer Analysis of Connexin 43 as a Potential Biomarker and Therapeutic Target in Human Kidney Renal Clear Cell Carcinoma (KIRC).Medicina (Kaunas, Lithuania) · 2024Article
- CX43 down-regulation promotes cell aggressiveness and 5-fluorouracil-resistance by attenuating cell stiffness in colorectal carcinoma.Cancer biology & therapy · 2023Article
- Connexins and Glucose Metabolism in Cancer.International journal of molecular sciences · 2022Review
- Intercellular delivery of therapeutic oligonucleotides.Journal of drug delivery science and technology · 2022Article
- A Connexin-Based Biomarker Model Applicable for Prognosis and Immune Landscape Assessment in Lung Adenocarcinoma.Journal of oncology · 2022Article
- The global status of research in prostate cancer bone metastasis: A bibliometric and visualized analysis.Frontiers in medicine · 2022Article
- Tubulin Isotypes: Emerging Roles in Defining Cancer Stem Cell Niche.Frontiers in immunology · 2022Review
- Glucose-limiting conditions induce an invasive population of MDA-MB-231 breast cancer cells with increased connexin 43 expression and membrane localization.Journal of cell communication and signaling · 2021Article
- GJA1 promotes hepatocellular carcinoma progression by mediating TGF-β-induced activation and the epithelial-mesenchymal transition of hepatic stellate cells.Open medicine (Warsaw, Poland) · 2021Article
- Review
- Connexins in Cancer: Jekyll or Hyde?Biomolecules · 2020Review
- Mechanical stimuli and matrix properties modulate cancer spheroid growth in three-dimensional gelatin culture.Journal of the Royal Society, Interface · 2020Article
- Connexins-Therapeutic Targets in Cancers.International journal of molecular sciences · 2020Review
- MYC as a Multifaceted Regulator of Tumor Microenvironment Leading to Metastasis.International journal of molecular sciences · 2020Review
- Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For decades, cancer was associated with gap-junction defects. However, more recently it appeared that the gap junction proteins (connexins) could be re-expressed and participate to cancer cell dissemination during the late stages of tumor progression. Since primary tumors of prostate cancer (PCa) are known to be connexin deficient, it was interesting to verify whether their bone-targeted metastatic behaviour could be influenced by the re-expression of the connexin type (connexin43) which is originally present in prostate tissue and highly expressed in bone where it participates to the differentiation of osteoblastic cells. Thus, we investigated the effect of the increased Cx43 expression, by retroviral infection, on the metastatic behaviour of two well-characterized cell lines (PC-3 and LNCaP) representing different stages of PCa progression. It appeared that Cx43 differently behaved in those cell lines and induced different phenotypes. In LNCaP, Cx43 was functional, localized at the plasma membrane and its high expression was correlated with a more aggressive phenotype both in vitro and in vivo. In particular, those Cx43-expressing LNCaP cells exhibited a high incidence of osteolytic metastases generated by bone xenografts in mice. Interestingly, LNCaP cells were also able to decrease the proliferation of cocultured osteoblastic cells. In contrast, the increased expression of Cx43 in PC-3 cells led to an unfunctional, cytoplasmic localization of the protein and was correlated with a reduction of proliferation, adhesion and invasion of the cells. In conclusion, the localization and the functionality of Cx43 may govern the ability of PCa cells to metastasize in bones.
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