Results 301 to 310 of about 590,806 (400)

C1q+ Macrophage–Tumor Cell Interaction Promoted Tumorigenesis via GPR17/PI3K/AKT Pathway Induced DNA Hypermethylation in Nasopharyngeal Carcinoma

open access: yesAdvanced Science, EarlyView.
In the TME of NPC, C1q secreted by C1q+ TAMs interacted with GPR17 to activate PI3K/AKT signaling through strengthening GPR17 coupling PI3K and increasing calcium levels in tumor cells. The activated PI3K/AKT signaling further induces DNA hypermethylation to promote the malignancy and stemness of tumor cells.
Yunzhi Liu   +11 more
wiley   +1 more source

HPD is an RNA‐Binding Protein Sustaining Ovarian Cancer Cell Glycolysis, Tumor Growth, and Drug Resistance

open access: yesAdvanced Science, EarlyView.
HPD is identified as an RNA‐binding protein that promotes mRNA translation by binding to RRACH motifs via its double‐stranded RNA‐binding domains. This RNA‐binding activity critically sustains glycolysis in ovarian cancer cells. Disrupting HPD's RNA‐binding function effectively suppresses tumor growth and enhances therapeutic sensitivity, highlighting ...
Fei Xie   +21 more
wiley   +1 more source

SNORA74A Drives Self‐Renewal of Liver Cancer Stem Cells and Hepatocarcinogenesis Through Activation of Notch3 Signaling

open access: yesAdvanced Science, EarlyView.
Abstract Liver cancer stem cells (CSCs) account for tumor initiation, heterogeneity and therapy resistance. However, the role of small nucleolar RNAs (snoRNAs) in the regulation of liver CSCs remains largely unclear. Here, this work identifies a conserved H/ACA box snoRNA SNORA74A which is highly expressed in liver CSCs.
Ziheng Zhou   +12 more
wiley   +1 more source

m6A‐Mediated TMCO3 Promotes Hepatocellular Carcinoma Progression by Facilitating the Membrane Translocation and Activation of AKT

open access: yesAdvanced Science, EarlyView.
TMCO3 as a downstream target of ALKBH5 is found, which regulates its expression in an m6A‐dependent manner, and then a new phosphorylation site on TMCO3 is identified and determines the specific mechanism of TMCO3 with AKT. Moreover, the combined treatment of targeting the TMCO3 and inhibition of AKT in mice models with HCC achieves great results ...
Xinxin Li   +8 more
wiley   +1 more source

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