Results 51 to 60 of about 462,862 (298)
COMP–PMEPA1 axis promotes epithelial‐to‐mesenchymal transition in breast cancer cells
This study reveals that cartilage oligomeric matrix protein (COMP) promotes epithelial‐to‐mesenchymal transition (EMT) in breast cancer. We identify PMEPA1 (protein TMEPAI) as a novel COMP‐binding partner that mediates EMT via binding to the TSP domains of COMP, establishing the COMP–PMEPA1 axis as a key EMT driver in breast cancer.
Konstantinos S. Papadakos +6 more
wiley +1 more source
Insulin-Like Growth Factor-I and Insulin-Like Growth Factor Binding Protein-3 in Alzheimer's Disease [PDF]
Few large studies have been conducted to assess the relationship between circulating IGF and late-life cognition.The aim of the study was to assess the relationship between IGF-I and IGF binding protein-3 (IGFBP-3) serum levels and cognitive impairment, including Alzheimer's disease (AD).In this multicentric cross-sectional study, 694 elderly subjects (
Duron, Emmanuelle +12 more
openaire +3 more sources
Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer
Dysregulation of the Hippo pathway drives nuclear accumulation of YAP/TAZ, activating stemness‐related transcriptional programs that sustain breast cancer stemness and fuel therapeutic resistance across subtypes, underscoring Hippo signaling as a targetable vulnerability. Figure created and edited with BioRender.com.
Giulia Schiavoni +11 more
wiley +1 more source
Background: miR-21 is overexpressed in many human cancers, including glioblastoma. Results: Insulin-like growth factor (IGF)-binding protein-3 (IGFBP3) is a novel miR-21 target gene and inhibits gliomagenesis in vitro and in vivo. Conclusion: miR-21 down-
Chuanhe Yang +10 more
semanticscholar +1 more source
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis +3 more
wiley +1 more source
Insulin-like growth factor I and insulin-like growth factor binding protein 5 in Crohn's disease [PDF]
Insulin-like growth factor (IGF)-I and its binding protein IGF binding protein 5 (IGFBP-5) were highly expressed in inflamed and fibrotic intestine in experimental Crohn's disease. IGF-I induced proliferation and increased collagen synthesis by smooth muscle cells and fibroblasts/myofibroblasts in vitro.
E M, Zimmermann +4 more
openaire +2 more sources
Insulin-like growth factor family and its impact on pulmonary arterial hypertension: a review
Pulmonary arterial hypertension (PAH) is a progressive and life-threatening cardiopulmonary disorder with rising global prevalence and limited curative options.
Nuo Li, Nuo Li, Degang Mo, Hongyan Dai
doaj +1 more source
MITF maintains genome stability in nonmelanocyte lineages
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir +13 more
wiley +1 more source
Nicole C Steiger-Luther1, Houda Darwiche1, Seh-Hoon Oh1, Jennifer M Williams1, Bryon E Petersen1,21Department of Pathology, Immunology and Laboratory Medicine, 2Program in Stem Cell Biology and Regenerative Medicine, College of Medicine, University of ...
Nicole C Steiger-Luther +3 more
doaj
Elevated C-peptide and insulin predict increased risk of colorectal adenomas in normal mucosa
Background Lower concentrations of the insulin like growth factor binding protein-1 (IGFBP-1) and elevated concentrations of insulin or C-peptide have been associated with an increase in colorectal cancer risk (CRC).
Vidal Adriana C +9 more
doaj +1 more source

