Aberrant FGF2/FGFR signaling is implicated in lung squamous cell carcinoma (LSCC), posing treatment challenges due to the lack of targeted therapeutic options. Designing drugs that block FGF2 signaling presents a promising strategy different from traditional kinase inhibitors. We previously reported a ColVα1-derived fragment, HEPV (127AA), that inhibits FGF2-induced angiogenesis.
View Article and Find Full Text PDFBackground: G-quadruplex DNA (G4) is a non-canonical structure forming in guanine-rich regions, which play a vital role in cancer biology and are now being acknowledged in both nuclear and mitochondrial (mt) genome. However, the impact of G4-based targeted therapy on both nuclear and mt genome, affecting mt function and its underlying mechanisms remain largely unexplored.
Methods: The mechanisms of action and therapeutic effects of a G4-binding platinum(II) complex, Pt-ttpy, on mitochondria were conducted through a comprehensive approaches with in vitro and in vivo models, including ICP-MS for platinum measurement, PCR-based genetic analysis, western blotting (WB), confocal microscope for mt morphology study, extracellular flux analyzer, JC1 and Annexin V apoptosis assay, flow cytometry and high content microscope screening with single-cell quantification of both ROS and mt specific ROS, as well as click-chemistry for IF study of mt translation.
Biochim Biophys Acta Mol Cell Res
July 2022
Basic FGF (bFGF) was discovered as a typical inducer of angiogenesis and has already been studied for 3 decades. Recent evidence indicates that bFGF plays different roles and controls signaling pathways that participate in the hallmarks of cancer, underscoring bFGF an appealing target for anti-cancer therapy. However, the early clinical trials designed to block bFGF signaling showed safety without satisfiable benefits for cancer patients.
View Article and Find Full Text PDF