Minzhi Sheng

ORCID: 0000-0002-5668-1314
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About
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Research Areas
  • Protease and Inhibitor Mechanisms
  • Signaling Pathways in Disease
  • Prostate Cancer Treatment and Research
  • Mesenchymal stem cell research
  • Cancer, Hypoxia, and Metabolism
  • Cancer Genomics and Diagnostics
  • Immunotherapy and Immune Responses
  • Nanoplatforms for cancer theranostics
  • Cancer Research and Treatments
  • Reproductive System and Pregnancy
  • Preterm Birth and Chorioamnionitis
  • Nuclear Structure and Function
  • Extracellular vesicles in disease
  • Ubiquitin and proteasome pathways
  • Cancer Immunotherapy and Biomarkers

Sunnybrook Health Science Centre
2023-2025

University of Toronto
2023-2025

Sunnybrook Research Institute
2023-2025

ABSTRACT The isolation of extracellular vesicles (EVs) using currently available methods frequently compromises purity and yield to prioritize speed. Here, we present a next‐generation aqueous two‐phase system (next‐gen ATPS) for the EVs regardless scale volume that is superior conventional such as ultracentrifugation (UC) commercial kits. This made possible by two phases, one rich in polyethylene glycol (PEG) other dextran (DEX), whereby fully encapsulated lipid preferentially migrate...

10.1002/jev2.70058 article EN cc-by Journal of Extracellular Vesicles 2025-03-01

N6-methyladenosine (m6A), the most abundant internal RNA modification in humans, regulates aspects of processing. Prostate cancer is characterized by widespread transcriptomic dysregulation; therefore, we m6A landscape 162 localized prostate tumors with matched DNA, and protein profiling. abundance varied dramatically across tumors, global patterns emerging via complex germline–somatic cooperative regulation. Individual germline polymorphisms regulated abundance, cooperating somatic mutation...

10.1038/s41588-025-02128-y article EN cc-by-nc-nd Nature Genetics 2025-03-24

Abstract Non-coding RNA (ncRNA) and binding proteins (RBPs) primarily reside in the nucleus to regulate splicing, transcription, transcript stability. However, their role(s) cytoplasm were unclear until now. Evidence now suggests that ncRNAs within play an important role cancer invasion. In concert with MT1-MMP, a protease involved invadopodia formation, long non-coding RNAs (lncRNAs) RBPs form cytoplasmic complexes which we termed “R-bodies” are abundant invasive breast cells....

10.1158/1538-7445.am2024-3203 article EN Cancer Research 2024-03-22

Abstract Prostate cancer (PCa) is the second most prevalent among males, and 5-year survival rate for patients with metastatic PCa (mPCa) ~30%. Although significant progress has been made in improving mPCa patients, many of these experience relapse or systemic toxicities. Protein expression prostate-specific membrane antigen (PSMA), a common often targeted therapy, unfortunately lost later stages mPCa. In contrast, six transmembrane epithelial prostate 1 2 (STEAP1 STEAP2) are both...

10.1158/1538-7445.am2024-61 article EN Cancer Research 2024-03-22

Limited graft availability is a constant clinical concern. Hence, the umbilical cord (UC) an attractive alternative to autologous grafts. The UC inexhaustible tissue source, and its removal harmless part of standard care after birth baby. Minimal information exists regarding immunological profile whole when it considered be used as graft. We aimed characterize localization levels class I human leukocyte antigens (HLAs) understand allogenicity UC. Additionally, HLA-E HLA-G are putative...

10.3390/bioengineering10010110 article EN cc-by Bioengineering 2023-01-12

Invadopodia facilitate cancer cell extravasation, but the molecular mechanisms whereby invadopodia-specific proteases such as MT1-MMP are called to invadopodia unclear. In metastatic breast cells, was found associate with plectin, a cytolinker protein, and vimentin, an intermediate filament protein. Interestingly, complex formation between plectin launches formation, subtype we termed iplectin (i=invadopodial). iPlectin vimentin cooperate deliver invadopodia. Genetic depletion of siRNA...

10.2139/ssrn.4319531 preprint EN 2023-01-01
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