ArticleBreast cancer research : BCR2023
RHAMM regulates MMTV-PyMT-induced lung metastasis by connecting STING-dependent DNA damage sensing to interferon/STAT1 pro-apoptosis signaling.
Article in Breast cancer research : BCR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- RHAMM drives formation of polyploid cancer cells and confers resistance to ER-targeted therapy in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- CD168 Identifies Proliferating Pancreatic Islet Cells in Murine and Human.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- HMMR in human cancers: regulatory mechanism and biological function.Journal of translational medicine · 2025Review
- Nanocarrier-mediated modulation of cGAS-STING signaling pathway to disrupt tumor microenvironment.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- NInternational journal of biological sciences · 2025Article
- Receptor for Hyaluronan Mediated Motility (RHAMM)/Hyaluronan Axis in Breast Cancer Chemoresistance.Cancers · 2024Article
- Elevated RHAMM as a biomarker for predicting diabetic kidney disease in patients with type 2 diabetes.Clinical kidney journal · 2024Article
- Activated interferon response from DNA damage in multiple myeloma cells contributes to the chemotherapeutic effects of anthracyclines.Frontiers in oncology · 2024Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRHAMM is a multifunctional protein that is upregulated in breast tumors, and the presence of strongly RHAMM
methodsWe interrogated the metastatic functions of RHAMM using a loss-of-function approach by crossing the MMTV-PyMT mouse model of breast cancer susceptibility with Rhamm
resultsRhamm-loss does not alter initiation or growth of MMTV-PyMT-induced primary tumors but unexpectedly increases lung metastasis. Increased metastatic propensity with Rhamm-loss is not associated with obvious alterations in proliferation, epithelial plasticity, migration, invasion or genomic stability. SNV analyses identify positive selection of Rhamm
conclusionRHAMM expression-loss blunts STING-IFN signaling, which offers growth advantages under specific microenvironmental conditions of lung tissue. These results provide mechanistic insight into factors controlling clonal survival/expansion of metastatic colonies and has translational potential for RHAMM expression as a marker of sensitivity to interferon therapy.
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