ArticleNature communications2020
SH3RF3 promotes breast cancer stem-like properties via JNK activation and PTX3 upregulation.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 70 citations in OpenAlex.
- PTX3 facilitates tumor cell migration and invasion through the miR-1255b-2-3p/CYP2J2 axis in oral squamous cell carcinoma.Cancer cell international · 2026Article
- Article
- METTL13 mediated SAA1 translation maintains cancer stem cell behavior and promotes esophageal carcinoma progression.Journal of translational medicine · 2026Article
- A YAP/TAZ-CDC6 Axis Initiates and Maintains Malignant Transformation.Cancer science · 2026Article
- Distinct mechanisms of cell in breast cancer and their clinical implication.Cell biology and toxicology · 2025Review
- Interactions between LncRNAs and MAPK signaling pathways in the pathogenesis of breast cancer.Cancer cell international · 2025Review
- Breast cancer induces CD62LCell discovery · 2025Article
- The long pentraxin 3: the invisible loom weaving the warp and weft of tumor destiny.Frontiers in immunology · 2025Review
- Transcriptomic Profiles and Functional Correlates of Cancer-Related Fatigue: A Cross-Sectional Study in Women Undergoing Cancer Treatment.European journal of cancer care · 2025Article
- Single-cell sequencing reveals PTX3 involvement in ovarian cancer metastasis.Journal of ovarian research · 2024Article
- SPDYC serves as a prognostic biomarker related to lipid metabolism and the immune microenvironment in breast cancer.Immunologic research · 2024Article
- Resveratrol Enhances Antioxidant and Anti-Apoptotic Capacities in Chicken Primordial Germ Cells through m6A Methylation: A Preliminary Investigation.Animals : an open access journal from MDPI · 2024Article
- Review
- PTX3 promotes breast cancer cell proliferation and metastasis by regulating PKCζbreast cancer, pentraxin 3, protein kinase Cζ, proliferation, metastasis.Experimental and therapeutic medicine · 2024Article
- Aggresome formation promotes ASK1/JNK signaling activation and stemness maintenance in ovarian cancer.Nature communications · 2024Article
- Inactivation of pentraxin 3 suppresses M2-like macrophage activity and immunosuppression in colon cancer.Journal of biomedical science · 2024Article
- Low level of ARID1A contributes to adaptive immune resistance and sensitizes triple-negative breast cancer to immune checkpoint inhibitors.Cancer communications (London, England) · 2023Article
- A Systematic Compilation of Human SH3 Domains: A Versatile Superfamily in Cellular Signaling.Cells · 2023Review
- SCUBE2 mediates bone metastasis of luminal breast cancer by modulating immune-suppressive osteoblastic niches.Cell research · 2023Article
- CircNFIX stimulates the proliferation, invasion, and stemness properties of ovarian cancer cells by enhancing SH3RF3 mRNA stability via binding LIN28B.The Kaohsiung journal of medical sciences · 2023Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer stem-like cells (CSCs) are the tumorigenic cell subpopulation and contribute to cancer recurrence and metastasis. However, the understanding of CSC regulatory mechanisms remains incomplete. By transcriptomic analysis, we identify a scaffold protein SH3RF3 (also named POSH2) that is upregulated in CSCs of breast cancer clinical tumors and cancer cell lines, and enhances the CSC properties of breast cancer cells. Mechanically, SH3RF3 interacts with the c-Jun N-terminal kinase (JNK) in a JNK-interacting protein (JIP)-dependent manner, leading to enhanced phosphorylation of JNK and activation of the JNK-JUN pathway. Further the JNK-JUN signaling expands CSC subpopulation by transcriptionally activating the expression of Pentraxin 3 (PTX3). The functional role of SH3RF3 in CSCs is validated with patient-derived organoid culture, and supported by clinical cohort analyses. In conclusion, our work elucidates the role and molecular mechanism of SH3RF3 in CSCs of breast cancer, and might provide opportunities for CSC-targeting therapy.
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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.