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Updated: Jul 13, 2026

Lung Tumor Cell Recruitment Assay
Published on: February 26, 2019
Ron-receptor tyrosine kinase in tumorigenesis and metastasis
Mike A Leonis1, Megan N Thobe, Susan E Waltz
1University of Cincinnati College of Medicine, Department of Pediatrics, Cincinnati, OH 45267-0558, USA.
Abstract:
The Ron-receptor tyrosine kinase has been increasingly recognized for its tumorigenic potential in the last decade. Ron-receptor activation leads to the activation of common receptor tyrosine kinase downstream-signaling pathways, and most prominently in tumor models, activation of MAPK, PI3K and beta-catenin. Numerous experimental models of mammalian tumorigenesis have demonstrated that increased Ron-receptor activity correlates with increased tumorigenesis in a variety of organs of epithelial origin. The evidence for Ron as an oncogene in human tumor biology is growing. The Ron receptor is overexpressed and over activated in a large number of human tumors, and overexpression of Ron correlates with a worse clinical outcome for patients in at least two human cancer states, namely breast and bladder cancer. Several experimental approaches have been demonstrated to successfully block Ron activity and function, and given these convincing data, approaches to block Ron-receptor activity in targeted human cancers should prove to be fruitful in the setting of future clinical research trials.
Insights
The Ron receptor tyrosine kinase promotes tumor growth and is overexpressed in human cancers like breast and bladder cancer. Blocking Ron activity offers a promising therapeutic strategy for targeted cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Signal Transduction
Background:
- The Ron receptor tyrosine kinase (RTK) plays a significant role in tumorigenesis.
- Ron activation triggers downstream signaling pathways, including MAPK, PI3K, and beta-catenin.
- Increased Ron activity is linked to increased tumorigenesis in epithelial cancers.
Purpose of the Study:
- To review the oncogenic potential of the Ron receptor.
- To highlight the correlation between Ron overexpression and poor clinical outcomes in breast and bladder cancers.
- To discuss the therapeutic implications of targeting Ron activity.
Main Methods:
- Review of experimental models of mammalian tumorigenesis.
- Analysis of human tumor biology data regarding Ron receptor expression.
- Evaluation of experimental approaches to inhibit Ron activity.
Main Results:
- Ron receptor tyrosine kinase is increasingly recognized for its tumorigenic potential.
- Overexpression and overactivation of Ron are observed in numerous human tumors.
- Ron overexpression correlates with worse clinical outcomes in breast and bladder cancers.
Conclusions:
- Evidence supports Ron's role as an oncogene in human cancer.
- Targeting Ron receptor activity presents a promising strategy for future clinical cancer trials.
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