Choushi Wang
A5033106400- Prostate Cancer Treatment and Research
- Epigenetics and DNA Methylation
- Cancer Genomics and Diagnostics
- Renal and related cancers
- Protein Degradation and Inhibitors
- Cancer-related gene regulation
- Renal cell carcinoma treatment
- Ubiquitin and proteasome pathways
- RNA Research and Splicing
- Genomics and Chromatin Dynamics
- RNA modifications and cancer
- Cancer-related Molecular Pathways
- Cytokine Signaling Pathways and Interactions
- PARP inhibition in cancer therapy
- Cancer, Lipids, and Metabolism
- Signaling Pathways in Disease
- Microbial Metabolism and Applications
- Aquaculture disease management and microbiota
- melanin and skin pigmentation
- Radiopharmaceutical Chemistry and Applications
- Neuropeptides and Animal Physiology
- Cancer, Stress, Anesthesia, and Immune Response
Broad Institute
2025
The University of Texas Southwestern Medical Center
2020-2024
Southwestern Medical Center
2020-2024
Jackson Laboratory
2020
Icahn School of Medicine at Mount Sinai
2020
Memorial Sloan Kettering Cancer Center
2020
Wuhan University
2017
Emerging evidence indicates that various cancers can gain resistance to targeted therapies by acquiring lineage plasticity. Although genomic and transcriptomic aberrations correlate with plasticity, the molecular mechanisms enabling acquisition of plasticity have not been fully elucidated. We reveal Janus kinase (JAK)-signal transducer activator transcription (STAT) signaling is a crucial executor in promoting plasticity-driven androgen receptor (AR)-targeted therapy prostate cancer....
Metastatic prostate cancer is characterized by recurrent genomic copy number alterations that are presumed to contribute resistance hormone therapy. We identified CHD1 loss as a cause of antiandrogen in an vivo small hairpin RNA (shRNA) screen 730 genes deleted cancer. ATAC-seq and RNA-seq analyses showed resulted global changes open closed chromatin with associated transcriptomic changes. Integrative analysis this data, together CRISPR-based functional screening, four transcription factors...
Tumor mutational burden and heterogeneity has been suggested to fuel resistance many targeted therapies. The cytosine deaminase APOBEC proteins have implicated in the signatures of more than 70% human cancers. However, mechanism underlying how cancer cells hijack mediated mutagenesis machinery promote tumor heterogeneity, thereby foster therapy remains unclear. We identify SYNCRIP as an endogenous molecular brake which suppresses APOBEC-driven prostate (PCa). Overactivated APOBEC3B,...
Abstract Cancer cells exhibit phenotypical plasticity and epigenetic reprogramming that allows them to evade lineage-dependent targeted treatments by adopting lineage plasticity. The underlying mechanisms which cancer exploit the regulatory machinery acquire therapy resistance remain poorly understood. We identified zinc finger protein 397 (ZNF397) as a bona fide coactivator of androgen receptor (AR), essential for transcriptional program governing AR-driven luminal lineage. ZNF397...
Abstract The rapid emergence of resistance to targeted therapies poses a substantial challenge in managing various advanced cancers, including prostate cancer (PCa). extent which PCa cells can autonomously manipulate the tumor microenvironment (TME) and swiftly adapt therapeutic challenges remains inadequately understood. We have elucidated that exploit neurolysin, crucial regulator neuronal signaling, counter interventions. frequent absence neurolysin results increased WNT3A secretion into...
Abstract Prostate cancer (PCa) is primarily driven by aberrant Androgen Receptor (AR) signaling. Although there has been substantial advancement in antiandrogen therapies, resistance to these treatments remains a significant obstacle, often marked continuous or enhanced AR signaling resistant tumors. While the dysregulation of ubiquitination-based protein degradation process instrumental accumulation oncogenic proteins, including AR, molecular mechanism ubiquitination-driven largely...
Pyomelanin is the major constituent of pigment in melanogenic Aeromonas strains bacteria. However, eumelanin, synthesized from tyrosine via L-DOPA and polyphenol oxidases (PPOs), may also be present this genus since frequently detected culture fluids several species. To address question, we used a deletion mutant media strain WS, which pyomelanin synthesis completely blocked under normal conditions. When was supplied to medium, observed residual melanin accumulation, interpret as evidence...
Abstract Introduction: Prostate cancer is the second leading cause of cancer-related death in American men, primarily driven by its ability to evade therapeutic interventions. This study uncovers a novel paradigm where neurolysin, peptidase previously ascribed neuronal function, orchestrates tumor microenvironment (TME) interfacing with cellular motor proteins. interaction precipitates series events that not only fortify cells' survival but also underpin resistance antiandrogen therapies....
Abstract Background: Prostate cancer, particularly in its castration-resistant form (CRPC), frequently develops resistance to androgen receptor (AR)-targeted therapies. This involves complex factors, including tumor mutational burden and heterogeneity. APOBEC proteins, associated with mutagenesis DNA damage, are implicated this process. Our study centers on SYNCRIP, a key regulator of activity, investigates influence extrachromosomal (ecDNA) CRPC. Objective: research aims explore how SYNCRIP...
<div>Abstract<p>Cancer cells exhibit phenotypical plasticity and epigenetic reprogramming that allows them to evade lineage-dependent targeted treatments by adopting lineage plasticity. The underlying mechanisms which cancer exploit the regulatory machinery acquire therapy resistance remain poorly understood. We identified zinc finger protein 397 (ZNF397) as a <i>bona fide</i> coactivator of androgen receptor (AR), essential for transcriptional program governing...
<p>Table S5. Lineage-Specific and AR Target Gene Signatures</p>
<p>Table S6. Key Resources</p>
<p>Table S5. Lineage-Specific and AR Target Gene Signatures</p>
<p>Figure S1. ZNF397-deficiency has bifurcated effects on PCa with or without AR inhibition. Figure S2. The impact of protein and cistrome. S3. ZNF397 is required for the activation canonical transcriptional program. S4. ZNF397-KO impairs DHT-induced signaling activation. S5. promotes multilineage lineage plastic gene expression. S6. stem-like EMT-like programs. S7. led to induction TET2 downstream genes. S8. S9. AR-dependent vs AR-independent PCas. S10. Targeting TET2-driven...
<p>Table S4. Candidate Resistance Driver Genes in ZNF397-KO Cells</p>
<p>Table S6. Key Resources</p>
<p>Table S1. Significantly Altered AR ChIP-seq Peaks in ZNF397-KO Cells</p>
<p>Table S3. Significantly Enriched or Depleted Signaling Pathways in GSEA Analysis</p>
<div>Abstract<p>Cancer cells exhibit phenotypical plasticity and epigenetic reprogramming that allows them to evade lineage-dependent targeted treatments by adopting lineage plasticity. The underlying mechanisms which cancer exploit the regulatory machinery acquire therapy resistance remain poorly understood. We identified zinc finger protein 397 (ZNF397) as a <i>bona fide</i> coactivator of androgen receptor (AR), essential for transcriptional program governing...
<p>Table S2. Differentially Expressed Genes in ZNF397-KO Cells</p>
<p>Table S3. Significantly Enriched or Depleted Signaling Pathways in GSEA Analysis</p>
<p>Table S1. Significantly Altered AR ChIP-seq Peaks in ZNF397-KO Cells</p>
<p>Table S2. Differentially Expressed Genes in ZNF397-KO Cells</p>
<p>Figure S1. ZNF397-deficiency has bifurcated effects on PCa with or without AR inhibition. Figure S2. The impact of protein and cistrome. S3. ZNF397 is required for the activation canonical transcriptional program. S4. ZNF397-KO impairs DHT-induced signaling activation. S5. promotes multilineage lineage plastic gene expression. S6. stem-like EMT-like programs. S7. led to induction TET2 downstream genes. S8. S9. AR-dependent vs AR-independent PCas. S10. Targeting TET2-driven...