Search bioRxiv⌕ Search

bioRxiv · 10.1101/565648

Syndecan-1 facilitates breast cancer metastasis to the brain

Abstract

PurposeAlthough survival rates for patients with localized breast cancer have increased, patients with metastatic breast cancer still have poor prognosis. Understanding key factors involved in promoting breast cancer metastasis is imperative for better treatments. In this study, we investigated the role of syndecan-1 (Sdc1) in breast cancer metastasis. MethodsTo assess the role of Sdc1 in breast cancer metastasis, we silenced Sdc1 expression in the triple-negative breast cancer human MDA-MB-231 cell line and overexpressed it in the mouse mammary carcinoma 4T1 cell line. Intracardiac injections were performed in an experimental mouse metastasis model using both cell lines. In vitro transwell blood-brain barrier (BBB) and brain section adhesion assays were utilized to specifically investigate how Sdc1 promotes brain metastasis. A cytokine array was performed to evaluate differences in the breast cancer cell secretome when Sdc1 was silenced. ResultsSilencing expression of Sdc1 in breast cancer cells significantly reduced metastasis to the brain. Conversely, overexpression of Sdc1 increased metastasis to the brain. We found that the reduction in brain metastases with Sdc1 knockdown was likely due to reduced breast cancer cell migration across the BBB and adhesion to the perivascular regions of the brain. However, there was no change in attachment to brain endothelial cells or astrocytes. Loss of Sdc1 also led to changes in breast cancer cell-secreted cytokines, which may influence the BBB. ConclusionsTaken together, our study demonstrates a role for Sdc1 in promoting breast cancer metastasis to the brain. These findings suggest that Sdc1 supports breast cancer cell migration across the BBB through regulation of cytokines, which may modulate the BBB. Further elucidating this mechanism will allow for the development of therapeutic strategies to combat brain metastasis.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Sayyad, M. R., Puchalapalli, M., Vergara, N. G., Mosticone Wangensteen, S., Moore, M., Mu, L., Edwards, C., Anderson, A., Kall, S., Sullivan, M., Dozmorov, M., Singh, J., Idowu, M. O., Koblinski, J. E.. 2019-03-02. Syndecan-1 facilitates breast cancer metastasis to the brain. https://doi.org/10.1101/565648

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Psychoneuroimmunology of Viral Hepatitis and Hepatocellular Carcinoma: A Systematic Review and Meta-Analysis

Hepatocellular carcinoma (HCC) and viral hepatitis (VH) are recognized primarily as hepatic diseases, yet they impose a substantial neuropsychiatric disorders (NPDs) encompassing depression, anxiety, cognitive impairment, and fatigue. Whether these manifestations reflect psychological reactions or biologically grounded psychoneuroimmune dysfunction remains poorly understood. Here, we present a pre-registered systematic review and meta-analysis (PROSPERO 2026 CRD420251081757) synthesizing evidence from 24 studies combining psychosocial outcomes with immune dysregulation markers across HCC and VH populations. Bibliometric and network analyses identified a growing psychoneuroimmunology research hub linking cytokine signaling, microglial activation, blood-brain barrier (BBB) disruption, and gut-liver-brain axis dysregulation to the neuropsychiatric phenotype of these diseases. Meta-analysis revealed a pooled hazard ratio (HR) of 1.92 (95% CI: 1.09-3.39) for adverse outcomes in HCC and a pooled HR of 2.28 (95% CI: 1.48-3.52) for depression associated to genetic variants in VH. TNF-a, but not IL-6, showed a tendency toward lower levels in VH patients with versus without NPDs, suggesting differential inflammatory roles. The literature, however, remains fragmented by heterogeneous designs and a paucity of longitudinal data. A psychoneuroimmunological approach, integrating immune, endocrine, neural, and psychosocial dimensions, is essential for capturing the full systemic impact of HCC and VH and should inform future mechanistic research and multidisciplinary clinical strategies.

cancer biology↗

Nutrient Availability as a Driver of Transcriptome Reprogramming in Osteosarcoma

Background: Gene expression in mammalian cells is intricately regulated by environmental and metabolic cues. Among these, nutrient availability represents a key feature of the tumor microenvironment and has recently emerged as a potent modulator of oncogenic signaling networks. In this study, we employed a cell-line model of osteosarcoma, a rare but highly aggressive bone malignancy affecting both humans and dogs. We demonstrate that altering the concentration of a single nutrient can profoundly reprogram gene expression in osteosarcoma cells, revealing a previously underexplored phenomenon: nutrient-dependent gene regulation. This finding highlights potential opportunities for therapeutic intervention and underscores the broader implications of metabolic regulation for personalized medicine and nutrition. Methods/Results: We performed bulk RNA sequencing of an established osteosarcoma cell line cultured under varying concentrations of two key nutrients, glucose and glutamine. Differential gene expression analysis revealed a pronounced nutrient-dependent transcriptional response. The identified genes were functionally associated with pathways involved in cancer, development, nervous system regulation, metabolism, cellular signaling, and immune responses. We identified seven distinct expression patterns, one of which exhibited a striking correlation with cell growth rate and resembled a FOS-like transcriptional signature. Notably, the proto-oncogene FOS was among the identified genes and displayed a strong growth-rate-dependent expression pattern. Conclusion/Impact: Our findings demonstrate that modulation of nutrient availability profoundly reshapes the gene expression landscape of osteosarcoma cells, revealing nutrient-responsive targets with potential therapeutic relevance. This work expands our understanding of metabolic regulation in cancer and suggests that nutrient-based interventions may provide a controllable means of influencing tumor progression. Beyond oncology, such approaches may also have broader implications for developmental biology, autoimmune disorders, and nervous system function. More broadly, this study highlights the potential of metabolic interventions as a strategy for targeted modulation of gene expression programs.

cancer biology↗

Synthetic chromatin engineering for STAT1 reactivation toward restoring cisplatin sensitivity in breast cancer

Chemoresistant cancers acquire transcriptomic and epigenetic alterations through changes in transcription factor activity and chromatin accessibility. Integrative in silico analyses identified STAT1 as a recurrently suppressed transcription factor in cisplatin-resistant breast cancer. Using cisplatin-resistant triple-negative breast cancer (TNBC) MDA-MB-231 cells, we further confirmed reduced STAT1 expression and activity, accompanied by defective nuclear translocation, indicating that suppression of STAT1 signaling contributes to cisplatin resistance in breast cancer. To restore STAT1 activity, we sought to promote its nuclear localization and transcriptional activation through chromatin engineering. Based on the identification of PHF6 as a direct STAT1-binding protein through in silico and in vitro analyses, we engineered Dual Reader 3 (DR3), a PHF6-derived synthetic chromatin regulator designed to enhance both STAT1 interaction and chromatin engagement through histone H2B ubiquitination. DR3 induced STAT1-associated transcriptional programs, including inflammatory and tumor-suppressive miRNAs. Mechanistically, DR3 physically promoted STAT1 nuclear translocation, activated STAT1 through a non-canonical S727-dependent mechanism independent of Tyr701 phosphorylation, and enhanced chromatin accessibility at STAT1-responsive regulatory regions through histone H2B ubiquitination. CUT&RUN analysis further revealed coordinated transcriptional and epigenetic remodeling associated with DR3-mediated STAT1 activation, including upregulation of HIPK2, which enhanced cellular sensitivity to cisplatin by strengthening the intrinsic DNA damage response. Finally, we investigated whether STAT1 reactivation could alleviate acquired cisplatin resistance. In vivo delivery of DR3 restored cisplatin sensitivity in resistant breast tumors. By coupling STAT1 nuclear translocation with chromatin remodeling, DR3 reactivated STAT1-dependent transcriptional programs and restored cisplatin sensitivity in breast cancer. Together, this study establishes transcription factor reactivation through synthetic chromatin engineering as a potential therapeutic strategy for overcoming chemoresistance in solid tumors.

cancer biology↗