Search bioRxiv⌕ Search

bioRxiv · 10.1101/2025.01.21.632253

B7-H3 as a Dual Clinically Relevant Checkpoint and Antibody Drug Conjugate Target Expressed Across Adenocarcinoma and Neuroendocrine Prostate Cancers

Abstract

Background and ObjectivesCD276 (B7-H3) has recently emerged as a promising presumptive immune checkpoint inhibitor (ICI) and a potential antibody-drug conjugate (ADC) target for prostate cancer (PCa). We evaluated B7-H3 and 15 other clinically relevant ADC and ICI targets for expression at the RNA and protein level across the PCa continuum--hormone-sensitive, castration-resistant, and neuroendocrine. MethodsCCLE data analysis and western blot experiments were performed for quantifying RNA and protein expression variability across PCa cell lines. Inter- and intratumoral heterogeneity was evaluated by integrating single-cell RNA sequencing data across 595k cells and 102 patients, spanning the disease continuum. AR and B7-H3 knockouts of PCa cell lines were developed and investigated using R1881 and Enzalutamide to elucidate the AR-CD276 signaling pathway through qRT-PCR and flow cytometry. Key FindingsB7-H3 showed high expression in tumor and myeloid cells (tumor microenvironment - TME), lowest heterogeneity across all ADC and ICI targets, and was negatively regulated by androgen signaling. LimitationsFurther validation of ADC and ICI target protein expression in human samples and more exhaustive exploration of the AR-CD276 signaling cascade is required. ConclusionB7-H3 demonstrates the least susceptibility to selective pressure due to its stable expression across PCa disease states. Clinical ImplicationsB7-H3 represents an important ADC target for PCa due to its potential to minimize drug resistance and likely ability to be a valid target across the prostate cancer continuum. Additionally, its expression in myeloid cells supports a dual role as an ICI, further enhancing its therapeutic relevance. Graphical AbstractDiscovery of optimal checkpoints and antibody drug conjugates (ADCs) in Prostate Cancer (PCa). O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=150 SRC="FIGDIR/small/632253v1_ufig1.gif" ALT="Figure 1"> View larger version (69K): org.highwire.dtl.DTLVardef@1af1115org.highwire.dtl.DTLVardef@8a9d70org.highwire.dtl.DTLVardef@6659aeorg.highwire.dtl.DTLVardef@189e200_HPS_FORMAT_FIGEXP M_FIG C_FIG Patient SummaryIn this study, we demonstrate that prostate cancer expresses high amounts of a cell surface protein called B7-H3 both when first diagnosed and throughout various stages of metastatic disease. Furthermore, we demonstrate a clear and yet to be fully resolved cross-talk between B7-H3 and the androgen signaling pathway central to prostate cancer development. We conclude that B7-H3 is therefore a highly promising therapeutic cell surface protein expressed by prostate cancer due to its stable expression potentially leading to low selective pressure and reduced drug resistance--thereby having significant implications for clinical trial design and patient inclusion considerations. Advancing PracticePCa is a highly heterogeneous disease with an increasingly wide treatment landscape, governed by various factors including clinical covariates, histopathological features, and molecular factors. B7-H3 has recently emerged as a promising clinical target for immunotherapy in the localized setting and antibody drug targeting in the metastatic setting. Despite the clinical significance, B7-H3 expression has not yet been thoroughly evaluated against other clinically relevant immune checkpoint and antibody drug targets, especially along the continuum of PCa treatment stages--hormone sensitive, castration resistant, and neuroendocrine. To our knowledge, this is the first study to characterize B7-H3 in this continuum using representative cell lines and the largest collection of PCa patient single cell sequencing data yet assembled in the literature, thus accounting for the substantial heterogeneity across PCa disease states as well as between datasets. Take Home MessageThis article explores the therapeutic relevance of clinical stage ADC targets and immune checkpoints for Prostate Cancer (PCa). We show that B7-H3 is a highly promising therapeutic candidate for PCa due to its stable expression across various disease states.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Sharma, S., Mundhara, N., Tekoglu, E., Amaral, A., Lotan, T. L., Gu, P., Luo, J., Baraban, E. G., Lack, N. A., Shenderov, E.. 2025-01-24. B7-H3 as a Dual Clinically Relevant Checkpoint and Antibody Drug Conjugate Target Expressed Across Adenocarcinoma and Neuroendocrine Prostate Cancers. https://doi.org/10.1101/2025.01.21.632253

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

KEEP EXPLORING

Related preprints

Tet2-Clonal Hematopoiesis Promotes Whereas Dnmt3a-CH Inhibits Breast Cancer Progression During Aging

Clonal hematopoiesis of indeterminate potential (CHIP) driven by somatic mutations in blood cells increases with age and is associated with adverse outcomes in cancer patients. How CHIP mutations influence solid tumor progression remains unclear. Using inducible murine models of Dnmt3a- or Tet2-mutant CHIP combined with orthotopic syngeneic breast cancer models, we demonstrate that upon aging Dnmt3a-mutant CHIP prevents whereas Tet2-mutant CHIP drives breast cancer progression. Dnmt3a-mutant immune infiltrates established interferon-mediated MHCIIhigh tumor-associated macrophages (TAMs) that supported cytotoxic CD8+ T cell-mediated tumor rejection. In contrast, Tet2-mutant TAMs exhibited an inflammatory, immunosuppressive phenotype characterized by increased IL-1 and CXCL2 production, reduced MHCII expression, and impaired T cell recruitment and activation. Therapeutic blockade of IL-1R1 or CXCR2 reduced tumor progression in aged Tet2-mutant CHIP mice and partially restored anti-tumor immunity. These findings establish that the effects of CHIP on cancer are mutation- and age-dependent and identify IL-1/CXCL2-driven inflammation as a therapeutic vulnerability of tumor-promoting Tet2-mutant CHIP.

cancer biology↗

Single Nucleus Profiling Reveals Rewired Tumor-Immune-Stromal Cell Communication in Plasmacytoid Urothelial Carcinoma

Plasmacytoid urothelial carcinoma (PUC) is an aggressive histologic subtype of bladder cancer associated with worse patient outcomes and therapeutic response compared to conventional urothelial carcinoma (CUC). While recent work has demonstrated metastatic lymph nodes from PUC tumors have an inflamed phenotype, how the tumor microenvironment (TME) and crosstalk between tumor, stromal, and immune cells in primary PUC bladder tumors differs from those in CUC remains poorly understood. The impact of these differences on response to immunotherapy is also unknown. To understand TME differences between CUC and PUC and their impact on cell signaling, we performed single nucleus RNA sequencing on PUC and CUC tumors, as well as Xenium spatial transcriptomics on a mixed CUC / PUC tumor. We identified increased signaling between PUC-enriched, CDH1-low urothelial cells, immunosuppressive lipid-associated macrophages, and SFRP2+/CTHRC1+ fibroblasts in PUC tumors compared to CUC. Spatial transcriptomics identified increased macrophage infiltration in PUC histology and colocalization of PUC tumor cells, immunosuppressive macrophages, and SFRP2+ fibroblasts. Taken together, this study delineates PUC architecture and demonstrates interplay CDH1-low tumor cells, EMT, and immunosuppressive macrophages, identifying possible therapeutic vulnerabilities in PUC.

cancer biology↗

The Phospholipase A2 Activity of Peroxiredoxin 6 Protects Hepatocarcinoma Cells Against Ferroptosis and Mitophagy Impairment

Peroxiredoxin 6 (PRDX6) is a moonlighting protein that plays a key role in regulating redox homeostasis and lipid metabolism through its unique dual peroxidase and calcium-independent phospholipase A2 (iPLA2) activities. Here, we generated a stable HepG2 cell line harboring a D140A mutation to selectively ablate iPLA2 activity, and we compared its phenotype with that of wild-type (WT) and PRDX6-knockout (KO) cells. D140A exhibited low ROS leves, similar to WT cells, confirming that oxidative stress is due to peroxidase deficiency. In contrast, D140A cells displayed higher lipid peroxidation than WT cells, though significantly lower than that of KO cells. Furthermore, the D140A mutant mirrored the KO phenotype regarding intracellular ferrous iron accumulation, impaired lipid droplet biogenesis, and the downregulation of the key ferroptosis regulator GPX4. Mechanistically, integrated proteomic, lipidomic, and enzymatic analyses revealed that a deficiency in iPLA2 activity of PRDX6 disrupted the release of key lipid species necessary for cell structure and signaling. Consequently, organelles involved in lipid synthesis and trafficking, such as peroxisomes, endoplasmic reticulum, mitochondria and lipid droplet, were affected. Specifically, we found that mitochondria exhibited a reduction in cristae and a diminished capacity for mitophagy and autophagy, which ultimately makes cells much more susceptible to erastin-induced ferroptotic cell death. Taken together, our findings demonstrate that PRDX6 iPLA2 activity uniquely coordinates organelle lipid homeostasis and mitophagy to protect cancer cells from ferroptotic cell death. Consequently, the use of iPLA2 inhibitors such as MJ33, which decreased PRDX6 iPLA2 activity to a level comparable to the mutant D140A, could represent a promising therapeutic strategy for inducing ferroptotic cell death in hepatocellular carcinoma.

cancer biology↗