IGF binding protein 3 inhib 
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  • ||||||||||  Journal:  Unraveling IGFBP3-mediated m6A modification in fracture healing. (Pubmed Central) -  Mar 11, 2024   
    The IGFBP3/miR-23a-3p/SMAD5 axis plays a pivotal role in fracture healing, highlighting the relevance of m6A modification. IGFBP3's role in stabilizing miR-23a-3p expression through m6A modification offers a potential therapeutic target for enhancing fracture healing outcomes.
  • ||||||||||  Lynparza (olaparib) / Merck (MSD), AstraZeneca
    IGFBP3 promotes resistance to olaparib via modulating EGFR signaling in advanced prostate cancer (Section 15; Poster Board #12) -  Mar 14, 2023 - Abstract #AACR2023AACR_6087;    
    Future work will utilize OlapR models to study how the IGFBP3/EGFR/DNA-PKcs protein complex promotes the development of resistance. Understanding the role of IGFBP3 in PARPi resistance will enhance our ability to re-sensitize resistant CRPC to PARPi therapeutics.
  • ||||||||||  Journal:  IGFBP3 inhibits angiotensin II-induced aortic smooth muscle cell phenotypic switch and MMPs expression. (Pubmed Central) -  Apr 1, 2022   
    IGFBP3 inhibited Ang II-induced mAoSMCs phenotypic switch as evidenced by increased smooth muscle actin alpha 2 (ACTA2) and myosin heavy chain 11 (MYH11) expression and decreased secreted phosphoprotein 1 (SPP1) and vimentin expression. Taken together, the present study demonstrates the role of IGFBP3 in preserving AoSMCs contractile state and reducing MMP9 activation and thus promoting elastic fiber synthesis, which provides a better understanding of the pathogenesis of TAD.
  • ||||||||||  Journal:  Downregulation of LOX promotes castration-resistant prostate cancer progression via IGFBP3. (Pubmed Central) -  Jan 11, 2022   
    The preclinical study in a mouse model suggested that introducing back LOX inhibited the progression of CRPC. In summary, we identified a new function of LOX in PCa and discovered that LOX downregulation contributed to progression via IGFBP3, and that the restoration of LOX may be a promising therapeutic strategy for PCa.
  • ||||||||||  Journal:  Senescent cells suppress innate smooth muscle cell repair functions in atherosclerosis. (Pubmed Central) -  Nov 10, 2021   
    SNCs do so by antagonizing IGF-1 through the secretion of insulin-like growth factor-binding protein 3 (Igfbp3). These data indicate that the intermittent use of senolytic agents or IGFBP-3 inhibition in combination with lipid lowering drugs may provide therapeutic benefit in atherosclerosis.
  • ||||||||||  Journal:  IGFBP-3 and TGF-β inhibit growth in epithelial cells by stimulating type V TGF-β receptor (TβR-V)-mediated tumor suppressor signaling. (Pubmed Central) -  Sep 7, 2021   
    By Western blot/phosphorimager/immunofluorescence-microscopy analyses, IGFBP-3 and TGF-β stimulate TβR-V-mediated IRS-2-dependent activation and cytoplasm-to-nucleus translocation of PP2A and PP1, resulting in dephosphorylation of p130/p107 and pRb, respectively, and growth arrest. Small molecule TGF-β enhancers, which potentiate TGF-β growth inhibition by enhancing TβR-I-TβR-II-mediated canonical signaling and thus activating TβR-V-mediated tumor suppressor signaling cascade (TβR-V/IRS-2/PP1/pRb), could be used to prevent and treat carcinoma.
  • ||||||||||  Journal:  The downregulation of IGFBP3 by TGF-β signaling in oral cancer contributes to the osteoclast differentiation. (Pubmed Central) -  Apr 20, 2021   
    Although IGFBP3 increased the viability of murine bone marrow macrophages, the osteoclast differentiation of these cells was blocked by IGFBP3 in a dose-dependent manner. These results revealed a novel pathway for the regulation of osteoclastogenesis by oral cancer cells, which may be a new therapeutic target for osteolysis induced by oral cancer infiltrating into the bone.