Results 181 to 190 of about 3,132,133 (305)

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, Sławomir Lasota, Ewelina Madej, Anna A. Brożyna, Małgorzata Szczygieł, Agnieszka Harazin‐Lechowska, Jan Czerbniak, Janusz Rys, Jaroslaw Czyz, Agnieszka Wolnicka‐Glubisz   +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, Gilar Gorji‐bahri, Lejla Gradjan, Julia Zajac, Kacper Gil, Yvonne Thokozile Nduku, Anna M. Blom   +6 more
wiley   +1 more source

Engineered extracellular vesicles enriched with the miR‐214/199a cluster enhance the efficacy of chemotherapy in ovarian cancer

Molecular Oncology, EarlyView.
Loss of the miR‐214/199a cluster is associated with recurrence in ovarian cancer. Engineered small extracellular vesicles (m214‐sEVs) elevate miR‐214‐3p/miR‐199a‐5p in tumor cells, suppress β‐catenin, TLR4, and YKT6 signaling, reprogram tumor‐derived sEV cargo, reduce chemoresistance and migration, and enhance carboplatin efficacy and survival in ...
Weida Wang, Ayesha Alvero, Yi Qin, Mingjin Wang, Alexandra Fox, Yanfeng Li, Michael Millman, Amy Kemper, Gil Mor, Xian Shuang Liu, Michael Chopp, Zheng Gang Zhang, Yi Zhang   +12 more
wiley   +1 more source

IMPDH inhibition enhances cytarabine efficacy in SAMHD1‐expressing leukaemia cells via guanine nucleotide depletion

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, Christopher Dirks, Caroline Eiden, Sonja K. Fesenmayer, Femke M. Hormann, Yolande Klootsema, Ingrid Lilienthal, Si Min Zhang, Nikolas Herold, Sean G. Rudd   +9 more
wiley   +1 more source

Keratin 19 as a prognostic marker and contributing factor of metastasis and chemoresistance in high‐grade serous ovarian cancer

Molecular Oncology, EarlyView.
Keratin 19 (KRT19) is overexpressed in high‐grade serous ovarian cancer with high levels of Kallikrein‐related peptidases (KLK) 4–7 and is associated with poor survival. In vivo analyses demonstrate that elevated KRT19 increases peritoneal tumour burden.
Sophia Bielesch, Isabel Vogel, Sina Nokodian, Johanna Moeller, Antonia Blechschmidt, Vicky Hecht, Vanessa Kuentzel, Katharina Thiedig, Melissa Schwab, Oliver Schilling, Holger Bronger, Marion Kiechle, Viktor Magdolen, Tobias Dreyer   +13 more
wiley   +1 more source

Dual PI3K/AKT and CDK4/6 inhibition reveals selective sensitivity in an SHH medulloblastoma stem cell model

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, Madeleine Birgersson, Paolo Ceriani, Margareta Wilhelm, Ourania N Kostopoulou   +4 more
wiley   +1 more source

Establishment of a humanized patient‐derived xenograft mouse model of high‐grade serous ovarian cancer for preclinical evaluation of combination immunotherapy

Molecular Oncology, EarlyView.
We have established a humanized orthotopic patient‐derived xenograft (Hu‐oPDX) mouse model of high‐grade serous ovarian cancer (HGSOC) that recapitulates human tumor–immune interactions. Using combined anti‐PD‐L1/anti‐CD73 immunotherapy, we demonstrate the model's improved biological relevance and enhanced translational value for preclinical ...
Luka Tandaric, Line Bjørge, Martine Rott Lode, Cecilie Fredvik Torkildsen, Pia Aehnlich, Rammah Elnour, Daniela Elena Costea, Lars Andreas Akslen, Liv Cecilie Vestrheim Thomsen, Emmet McCormack, Katrin Kleinmanns   +10 more
wiley   +1 more source

Deciphering transcriptional plasticity in pancreatic ductal adenocarcinoma reveals alterations in sensory neuron innervation

Molecular Oncology, EarlyView.
Pancreatic sensory neurons innervating healthy and PDAC tissue were retrogradely labeled and profiled by single‐cell RNA sequencing. Tumor‐associated innervation showed a dominant neurofilament‐positive subtype, altered mitochondrial gene signatures, and reduced non‐peptidergic neurons.
Elena Genova, Michele Montrone, Uday Rangaswamy, Francesco Diversi, Irene Schiavo, Denise Ferrarini, Roberta Di Florio, Irene Longo, Michele Coscia, Nicola Zamboni, Giorgia Demontis, Lisa Veghini, Vincenzo Corbo, Remo Sanges, Paul Heppenstall   +14 more
wiley   +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, Shiva Krishna Katkam, Zhefan Wang, Venkateshwar G. Keshamouni   +3 more
wiley   +1 more source

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

Molecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu, Xixi Lin, Emil Mladenov, Veronika Mladenova, Jürgen Thomale, Ali Sak, Yao Wang, Yunxuan Deng, Eleni Gkika, Martin Stuschke, George Iliakis   +10 more
wiley   +1 more source