ArticleBiology direct2024
The RRP9-JUN axis promotes breast cancer progression via the AKT signalling pathway.
Article in Biology direct, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Multimodal deep learning for predicting neoadjuvant treatment outcomes in breast cancer: a systematic review.Biology direct · 2025Pooled it
- Biologically-informed integration of drug representations for breast cancer treatment using deep learning.Nature communications · 2025Trial
- Pre-Regenerative Endothelial Cells Empowered by Antler Blood Exosomes Orchestrate Peripheral Nerve Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- RRP9 suppresses hepatocellular carcinoma progression by inhibiting the PI3K/AKT/mTOR pathway.International journal of oncology · 2026Article
- Emerging Approaches in Breast Cancer: From Molecular Mechanisms to Diagnosis and Therapeutic Strategies.Oncology research · 2026Review
- Harnessing Ribonucleoprotein Granule Biology for Cancer Therapy: The Central Role of Protein Modifications.Research (Washington, D.C.) · 2026Review
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Authors and funding
6 authors.
Funding
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Abstract
backgroundRibosomal RNA processing 9 (RRP9) is a specific component of the U3 small nucleolar ribonucleoprotein (U3 snoRNP), which is involved in physiological processes and pathological disorders. The purpose of the current study was to investigate the biological roles of RRP9 in breast cancer (BC) progression.
methodsThe expression levels of RRP9 in human BC were assessed by immunohistochemical (IHC) staining, qPCR assay and Western blot. Cells were transfected with shRNA plasmids to regulate RRP9 expression. The functional roles were explored by Celigo cell counting assay, colony formation assay, flow cytometry and Transwell assays, as well as construction of Xenograft tumor model. Furthermore, interaction between RRP9 and JUN was determined by Co-immunoprecipitation (Co-IP) assay, protein stability assay, and ubiquitination assay.
resultsRRP9 expression was substantially upregulated in BC tissues and was positively associated with lymph node metastasis and poor prognosis. Functional experiments indicated that RRP9 depletion inhibited BC progression both in vitro and in vivo. Using a prime-view human gene expression array and IPA, JUN was identified as a potential downstream target of RRP9. Mechanistically, RRP9 interacted with the JUN protein, and RRP9 deletion decreased JUN protein stability by accelerating JUN ubiquitination and led to JUN degradation via MDM2. Moreover, the regulatory effects of RRP9 on BC cell phenotypes were attenuated by JUN knockdown or the AKT signalling pathway activator SC79.
conclusionsIn conclusion, this study revealed the crucial role of RRP9 in BC progression and its probable novel mechanism, suggesting that RRP9 may be a promising candidate for the treatment of BC.
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