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Pi3k/akt/mtor Signaling in Cancer / Cancer Cells and Metastasis / Mechanisms of Cancer Metastasis · Journal article
Biomarker Research · August 10, 2026
Early or partial results. Treat as a signal, not a conclusion.
This is a preclinical mechanistic study identifying RBM38 as a suppressor of breast cancer stemness and developing an ASCP-based protein delivery platform in transgenic mice and PDX models. The work elucidates phosphorylation-dependent regulation of RBM38 and demonstrates proof-of-concept tumor localization and stemness reduction in xenografts, but no human clinical efficacy data are presented.
Preclinical mechanistic study in transgenic mice and patient-derived xenograft models. MMTV-PyMT transgenic mice with breast cancer, patient-derived xenograft models, and human tissue samples for mechanism validation. Intervention: Targeted RBM38 expression in breast tissue; ASCP-RBM38 delivery platform in PDX models. Compared with: Doxorubicin co-administration (for cardiotoxicity assessment); no explicit control comparator stated for efficacy endpoints.
RBM38 expression decreases during breast cancer progression in MMTV-PyMT transgenic mice Targeted RBM38 expression suppressed tumor initiation, decreased tumor size and metastasis, and reduced breast cancer stem cells Phosphorylation of RBM38 at Ser117, Thr120, and Thr132 by SLK and PGAM5 is required for stemness suppression and HOXD10 mRNA regulation
ASCP-RBM38 achieved effective tumor localization in PDX models and protected against doxorubicin-induced cardiotoxicity
This work is pre-clinical and does not yet support clinical recommendations. It provides a mechanistic rationale and delivery platform for RBM38 restoration as a potential breast cancer stem cell-targeting therapy, pending human trial data.
Preclinical mechanistic study in transgenic mice and PDX models with a novel protein delivery approach; no clinical efficacy data or human trials reported, only mechanism validation and proof-of-concept in xenografts.
As stated by the source record.
This work is pre-clinical and does not yet support clinical recommendations. It provides a mechanistic rationale and delivery platform for RBM38 restoration as a potential breast cancer stem cell-targeting therapy, pending human trial data.
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What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Breast cancer stemness drives tumor progression and therapy resistance, yet the underlying mechanisms remain poorly understood. In this study, we observed that RBM38 expression gradually decreases during breast cancer progression in MMTV - PyMT transgenic mice. Using a model with targeted RBM38 expression in breast tissue, we found it suppressed tumor initiation, decreased tumor size and metastasis, and reduced breast cancer stem cells. Multi-omics analyses, including single-cell and spatial transcriptomics, RIP-sequencing, and proteomics, were used to reveal the mechanisms. We identified HOXD10 mRNA as a critical downstream target of RBM38. Phosphorylation of RBM38 at Ser117, Thr120, and Thr132 by SLK and PGAM5 is required for RBM38-mediated stemness suppression, protein complex formation, and HOXD10 mRNA regulation. Based on these insights, we explored RBM38’s therapeutic potential using an activatable supercharged polypeptide (ASCP) delivery platform. In patient-derived xenograft (PDX) models, ASCP-RBM38 achieved effective tumor localization, reduced stemness, and protected against doxorubicin (DOX)-induced cardiotoxicity. Clinical analysis of human samples validated this mechanism. Our study underscores the pivotal role of phosphorylation-mediated regulation and protein complex formation in RBM38-mediated control of breast cancer stemness, highlighting its therapeutic potential.
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