Results 111 to 120 of about 1,477,881 (298)
RIPK4 function interferes with melanoma cell adhesion and metastasis
Molecular Oncology, EarlyView.RIPK4 promotes melanoma growth and spread. RIPK4 levels increase as skin lesions progress to melanoma. CRISPR/Cas9‐mediated deletion of RIPK4 causes melanoma cells to form less compact spheroids, reduces their migratory and invasive abilities and limits tumour growth and dissemination in mouse models.
Norbert Wronski +9 more
wiley +1 more source
COMP–PMEPA1 axis promotes epithelial‐to‐mesenchymal transition in breast cancer cells
Molecular Oncology, EarlyView.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
Microbiology and Molecular Biology Reviews, 2004 Philippe P Roux, J. Blenis
semanticscholar +1 more source
Molecular Oncology, EarlyView.Cytarabine is a key therapy for acute myeloid leukaemia (AML), but its efficacy is limited by the dNTPase SAMHD1, which hydrolyses its active metabolite. Screening nucleotide biosynthesis inhibitors revealed that IMPDH inhibitors selectively sensitise SAMHD1‐proficient AML cells to cytarabine.
Miriam Yagüe‐Capilla +9 more
wiley +1 more source
Molecular Oncology, EarlyView.Targeted therapy was evaluated in SHH medulloblastoma using neuroepithelial stem cell (NES) and tumor‐derived NES‐like (tNES) models in 2D monolayers and 3D spheroids. PI3K, AKT, and CDK4/6 inhibitors had minimal effects in NES but markedly reduced viability and growth and induced apoptosis in tNES cells, revealing distinct therapeutic vulnerabilities.
Monika Lukoseviciute +4 more
wiley +1 more source
MAP kinase kinase kinase kinase 3 (MAP4K3; GLK) [PDF]
Science-Business eXchange, 2011 openaire +1 more source
E2A selectively regulates TGF‐β–induced apoptosis in KRAS‐mutant non‐small cell lung cancer
Molecular Oncology, EarlyView.Ability to induce apoptosis by TGF‐β is frequently lost in advanced lung adenocarcinoma despite intact TGF‐β signaling. We identify E2A as a mutant KRAS–dependent mediator of resistance to TGF‐β–induced apoptosis. TGF‐β induces E2A via SMAD3 in mutant KRAS cells, and E2A silencing restores apoptosis and enhances radiation response in cell lines ...
Sergei Chuikov +3 more
wiley +1 more source