Results 131 to 140 of about 153,560 (299)

On the Local Structure of Water Surrounding Inorganic Anions Within Layered Double Hydroxides

Molecules
Understanding the microscopic structure and physical–chemical properties of materials with nanoconfined domains is essential for advancing technologies in catalysis, nanomaterial design, and pharmaceutical applications.
Abderrahmane Semmeq, Kanika Anand, Antoine Carof, Adolfo Bastida, Francesca Ingrosso   +4 more
doaj   +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

CCDC80 suppresses high‐grade serous ovarian cancer migration via negative regulation of B7‐H3

Molecular Oncology, EarlyView.
PAX8 is a lineage‐specific master regulator of transcription in high‐grade serous ovarian cancer (HGSC) progression. We show for the first time that PAX8 facilitates proliferation and metastasis by repressing the cell autonomous tumor suppressor CCDC80 and inducing B7‐H3 expression.
Aya Saleh, Nitzan Medina‐Itzhaki, Milena Chekov, Eden Gal‐Swisa, Roba Gabesh‐Wahabi, Inbar Savyon, Inna Naroditsky, Hilary A. Kenny, Basem Fares, Lina Korsensky, Einav Girsh, Liron Berger, Ruth Perets   +12 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

THERMODYNAMIC ASPECTS OF SOLVATION AND DILUTION FOR ACETANILIDE AND PHENACETIN IN SOME AQUEOUS AND ORGANIC SOLVENTS MUTUALLY SATURATED ASPECTOS TERMODINÁMICOS DE LA SOLVATACIÓN Y LA DILUCIÓN DE ACETANILIDA Y FENACETINA EN ALGUNOS SOLVENTES ORGÁNICOS Y ACUOSOS MUTUAMENTE SATURADOS

Vitae, 2008
Acetanilide (ACN) and phenacetin (PNC) are compounds structurally related with acetaminophen widely used as model drugs in pharmaceutical chemistry. Based on published thermodynamic quantities for dissolution, partitioning and sublimation of ACN and PNC,
Yolima BAENA A, Edgar F VARGAS E, Fleming MARTÍNEZ R   +2 more
doaj  

Adaptor protein CIN85 potentiates the motility of osteosarcoma cells via the Akt/mTOR and MMP2‐COL3A1 axis

Molecular Oncology, EarlyView.
CIN85 is highly expressed in osteosarcoma, particularly in metastatic lesions. Its overexpression increases cell migration and Matrigel invasion, while silencing CIN85 suppresses these behaviors. Transcriptome analysis shows that CIN85 regulates MMP2, COL3A1, and Akt/mTOR signaling. Targeting these pathways reverses CIN85‐induced motility, highlighting
Iryna Horak, Iva Staniczková Zambo, Matěj Přikryl, Peter Múdry, Danica Zapletalová, Jarmila Navrátilová, Jiří Navrátil, Jan Šmarda, Liudmyla Drobot, Petr Beneš, Lucia Knopfová   +10 more
wiley   +1 more source

Interaction of HS1BP3 with cortactin modulates TKS5 localisation, cell secretion and cancer malignancy

Molecular Oncology, EarlyView.
Here, we demonstrate that HS1BP3 interacts with Cortactin through a proline‐rich region (PRR3.1) and show that this interaction, and HS1BP3 itself, promote cancer cell proliferation and invasion. Inhibition of this interaction leads to build‐up of TKS5 in multivesicular endosomes and altered secretion of CD63 and CD9, providing an explanation for the ...
Arja Arnesen Løchen, Kristiane Søreng, Chiara Veroni, Laura Trachsel‐Moncho, Nagham Asp, Robin Gaupset, Lars Gustav Lyckander, Helene Knævelsrud, Lars Eftang, Anne Simonsen   +9 more
wiley   +1 more source

Insights into a long life without cancer: The case of the bowhead whale

Molecular Oncology, EarlyView.
Long‐lived, large‐bodied organisms have evolved powerful anticancer mechanisms that preserve cellular and tissue integrity across extended lifespans. A recent study by Firsanov et al. shows that greater genome stability is a key factor underlying the remarkable longevity and cancer resistance of one such species, the bowhead whale.
Inés Paniagua, Johanna A. Joyce
wiley   +1 more source

Proteasome inhibitor, ixazomib prevents topoisomerase‐I degradation and reverses irinotecan resistance in colorectal cancer

Molecular Oncology, EarlyView.
Ixazomib inhibits proteasome‐mediated degradation of topoisomerase I induced by irinotecan, thereby restoring drug sensitivity and promoting tumor cell death in colorectal cancer. Irinotecan, a topoisomerase I (topoI) inhibitor, is widely used for colorectal cancer, but resistance remains a major clinical challenge.
Yuho Ebata, Koji Ando, Hirofumi Hasuda, Koshi Mimori, Elizabeth C. Unan, Siddhartha Pulukuri, Aahana Tiku, Allison Berger, Eiji Oki, Ajit Bharti, Tomoharu Yoshizumi   +10 more
wiley   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

Molecular Oncology, EarlyView.
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, Jack V. Mills, Wojciech Niedzwiedz, Valentine M. Macaulay   +3 more
wiley   +1 more source