- |||||||||| 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: 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.
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