The insulin-like growth factor (IGF) system, which is constituted by the IGF-1 and IGF-2 peptide hormones, their corresponding receptors and several IGF binding proteins, is involved in physiological and pathophysiological processes. The IGF system promotes cancer proliferation/survival and its signaling induces the epithelial-mesenchymal transition (EMT) phenotype, which contributes to the migration, invasiveness, and metastasis of epithelial tumors. These cancers share two major IGF-1R signaling transduction pathways, PI3K/AKT and RAS/MEK/ERK. However, as far as we could review at this time, each type of cancer cell undergoes EMT through tumor-specific routes. Here, we review the tumor-specific molecular signatures of IGF-1-mediated EMT in breast, lung, and gastric cancers.
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http://dx.doi.org/10.3390/ijms19082411 | DOI Listing |
Nat Commun
January 2025
Robson DNA Science Centre, Charbonneau Cancer Institute, Department of Biochemistry & Molecular Biology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
To tolerate oxidative stress, cells enable DNA repair responses often sensitive to poly(ADP-ribose) (PAR) polymerase 1 and 2 (PARP1/2) inhibition-an intervention effective against cancers lacking BRCA1/2. Here, we demonstrate that mutating the CHD6 chromatin remodeler sensitizes cells to PARP1/2 inhibitors in a manner distinct from BRCA1, and that CHD6 recruitment to DNA damage requires cooperation between PAR- and DNA-binding domains essential for nucleosome sliding activity. CHD6 displays direct PAR-binding, interacts with PARP-1 and other PAR-associated proteins, and combined DNA- and PAR-binding loss eliminates CHD6 relocalization to DNA damage.
View Article and Find Full Text PDFJ Immunother Cancer
January 2025
Center for Immunotherapy, Roswell Park Comprehensive Cancer Center, Buffalo, New York, USA
Evidence has shown that T-cell receptors (TCRs) that recognize the same epitopes may not be the exact TCR clonotypes but have slightly different TCR sequences. However, the changes in the genomic and transcriptomic signatures of these highly homologous T cells during immunotherapy remain unknown. Here, we examined the evolutionary features in circulating TCR clonotypes observed in tumors (tumor-infiltrating lymphocyte (TIL)-TCRs) by combining single-cell RNA/TCR sequencing of longitudinal blood samples and TCR sequencing of tumor tissue from a patient treated with anti-cytotoxic T-lymphocyte-associated protein 4/programmed cell death protein-1 therapy.
View Article and Find Full Text PDFJ Biol Chem
January 2025
Department of Physiology, School of Medicine, University of Maryland Baltimore, Baltimore, MD, 21201, USA. Electronic address:
Sarcoplasmic/endoplasmic reticulum Ca-ATPase1 (SERCA1) is responsible for the clearance of cytosolic Ca in skeletal muscle. Due to its vital importance in regulating Ca homeostasis, the regulation of SERCA1 has been intensively studied. Small ankyrin 1 (sAnk1, Ank1.
View Article and Find Full Text PDFPlacenta
January 2025
Magee-Women's Research Institute, Department of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA, 15213, USA; Department of Microbiology and Molecular Genetics, University of Pittsburgh, Pittsburgh, PA, 15213, USA. Electronic address:
Introduction: Fusion of mononucleated cytotrophoblasts into syncytium leads to trophoblast senescence. Yet, premature senescence is associated with preeclampsia, fetal growth restriction (FGR), and related obstetrical syndromes. A set of 28 transcripts that comprise senescence-associated secretory phenotype (SASP) was recently described in placentas from women with preeclampsia.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Cheeloo College of Medicine, Shandong University, Jinan 250012, China; Department of Gastroenterology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining 272000, China. Electronic address:
Background: Ulcerative colitis (UC) is a persistent chronic, non-specific inflammatory disease, and macrophages play a crucial role in its pathogenesis. Spleen tyrosine kinase (Syk) is strongly associated with the pathogenesis of several inflammatory diseases. However, the role of Syk in the pathogenesis of UC is still obscure.
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