ArticleInternational journal of oncology2018
Effects of cell-cell crosstalk on gene expression patterns in a cell model of renal cell carcinoma lung metastasis.
Article in International journal of oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Myofibroblast depletion reduces kidney cyst growth and fibrosis in autosomal dominant polycystic kidney disease.Kidney international · 2023Article
- Vasopressin Receptor Type-2 Mediated Signaling in Renal Cell Carcinoma Stimulates Stromal Fibroblast Activation.International journal of molecular sciences · 2022Article
- Exploring cell-specific miRNA regulation with single-cell miRNA-mRNA co-sequencing data.BMC bioinformatics · 2021Article
- Insulin and insulin-like growth factors act as renal cell cancer intratumoral regulators.Journal of cell communication and signaling · 2019Article
- Metastatic Tumor Burden and Loci as Predictors of First Line Sunitinib Treatment Efficacy in Patients with Renal Cell Carcinoma.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The median survival rate of patients with metastatic renal carcinoma is approximately 10 to 12 months, with up to 50% of patients developing metastases in the lung parenchyma. The molecular basis for metastatic development remains unclear. In the present study, we used renal cell carcinoma (RCC) cells and bronchial epithelial cells, representing metastasis target organ cells, conditioned medium and co-culture models to identify specific gene expression changes responsible for cancer cell viability in a metastatic microenvironment. RCC cell proliferation and migration increased when the culture was supplemented with conditioned medium from lung fibroblasts or pleural epithelial cells. Healthy epithelial cells were, in turn, also stimulated with conditioned medium from RCC cell lines. The mitogen-activated protein kinase (MAPK), interleukin (IL)-6, and phosphatidylinositol 4,5-bisphosphate (PIP2) signaling pathways were identified as deregulated upon cell‑cell interaction. Thus, cell-cell communication may contribute to the development of the metastatic niche. The identified deregulated signaling pathways may be considered as potential therapeutic targets in metastatic renal carcinoma.
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Registered trials
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