Publications by authors named "Qinju He"

Article Synopsis
  • The study reveals that the RNA methylation enzyme METTL3 is overexpressed in prostate cancer (PCa), correlating with poorer patient outcomes and establishing it as a potential oncoprotein.
  • Researchers mapped the mA landscape in clinical samples and identified RRBP1 as a key target of METTL3, which enhances its stability in an mA-dependent way, contributing to aggressive PCa characteristics.
  • The team developed two METTL3 peptide inhibitors that effectively reduce cancer cell growth in lab settings and tumor growth in animal models, highlighting a promising therapeutic avenue in targeting the METTL3/mA/RRBP1 signaling pathway.
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Article Synopsis
  • PRMT5 is a key protein involved in arginine methylation linked to various biological functions and is often overexpressed in aggressive prostate cancer (PCa), where it negatively impacts patient survival and promotes cancer growth.* -
  • Inhibiting PRMT5 through genetic methods or drugs reduces cancer stemness and disrupts the cell cycle, demonstrating a stronger antitumor effect in more aggressive forms of PCa.* -
  • Combining PRMT5 inhibitors with anti-PD-1 immunotherapy shows greater effectiveness against castration-resistant PCa, and a global CRISPR/Cas9 screen reveals potential for repurposing existing drugs to enhance treatment when used alongside PRMT5 inhibitors.*
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Article Synopsis
  • Prostate cancer exhibits significant histopathological diversity, and a new subtype identified as small cell-like PCa (SCLPC) shows aggressive clinical behavior with low androgen receptor activity but high stemness and proliferation.
  • This subtype is characterized by a molecular profile associated with protein translation, including overexpression of ribosomal protein genes and SP1, a transcription factor linked to castration-resistant PCa (CRPC).
  • Targeted therapies like the SP1 inhibitor plicamycin and the translation elongation inhibitor homoharringtonine demonstrate potential in reducing CRPC growth and progression, highlighting these pathways as promising avenues for clinical treatment.
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The molecular mechanisms underpinning prostate cancer (PCa) progression are incompletely understood, and precise stratification of aggressive primary PCa (pri-PCa) from indolent ones poses a major clinical challenge. Here, we comprehensively dissect, genomically and transcriptomically, the mA ( -methyladenosine) pathway as a whole in PCa. Expression, but not the genomic alteration, repertoire of the full set of 24 mA regulators at the population level successfully stratifies pri-PCa into three mA clusters with distinct molecular and clinical features.

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Type 2 diabetes increases the risk for cancer. Centrosome amplification can initiate tumorigenesis. We have described that type 2 diabetes increases the centrosome amplification of peripheral blood mononuclear cells, with high glucose, insulin, and palmitic acid as the triggers, which suggests that centrosome amplification is a candidate biological mechanism linking diabetes to cancer.

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