Hypomethylation‐associated ELF3 helps nasopharyngeal carcinoma to escape immune surveillance via MUC16-mediated glycolytic metabolic reprogramming DOI
Yueyang Liu, Hong Zhou, Yu Qi

et al.

AJP Cell Physiology, Journal Year: 2024, Volume and Issue: 327(4), P. C1125 - C1142

Published: Sept. 2, 2024

Immune escape and metabolic reprogramming are two essential hallmarks of cancer. Mucin-16 (MUC16) has been linked to glycolysis immune response in different cancers. However, its involvement nasopharyngeal carcinoma (NPC) not well described. We seek dissect the functions detailed mechanisms MUC16 NPC. Bioinformatics prediction was performed identify NPC-related molecules. significantly enhanced NPC tissues, which correlated with advanced tumor stage patients. Lentiviral plasmids-mediated deletion inhibited malignant behavior cells, inhibition by blocked cells. E74-like factor 3 (ELF3) bound promoter promotes transcription MUC16. overexpression reversed repressive effect ELF3 silencing on accelerated growth vivo. Overexpression associated reduced DNA methylation promoter. Our findings revealed role ELF3/MUC16 axis NPC, providing potential therapeutic targets for

Language: Английский

The p-MYH9/USP22/HIF-1α axis promotes lenvatinib resistance and cancer stemness in hepatocellular carcinoma DOI Creative Commons

Qiaonan Shan,

Lu Yin,

Qifan Zhan

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2024, Volume and Issue: 9(1)

Published: Sept. 19, 2024

Language: Английский

Citations

10
ENPP1 Promotes Immune Suppression, Drug Resistance, and Adverse Outcomes in Bladder Cancer: Potential for Targeted Therapy DOI
Chengyu You,

Qixiang Fang,

Xi Xiao

et al.

Cancer Genetics, Journal Year: 2025, Volume and Issue: 294-295, P. 1 - 14

Published: March 4, 2025

Language: Английский

Citations

0
Hypomethylation‐associated ELF3 helps nasopharyngeal carcinoma to escape immune surveillance via MUC16-mediated glycolytic metabolic reprogramming DOI
Yueyang Liu, Hong Zhou, Yu Qi

et al.

AJP Cell Physiology, Journal Year: 2024, Volume and Issue: 327(4), P. C1125 - C1142

Published: Sept. 2, 2024

Immune escape and metabolic reprogramming are two essential hallmarks of cancer. Mucin-16 (MUC16) has been linked to glycolysis immune response in different cancers. However, its involvement nasopharyngeal carcinoma (NPC) not well described. We seek dissect the functions detailed mechanisms MUC16 NPC. Bioinformatics prediction was performed identify NPC-related molecules. significantly enhanced NPC tissues, which correlated with advanced tumor stage patients. Lentiviral plasmids-mediated deletion inhibited malignant behavior cells, inhibition by blocked cells. E74-like factor 3 (ELF3) bound promoter promotes transcription MUC16. overexpression reversed repressive effect ELF3 silencing on accelerated growth vivo. Overexpression associated reduced DNA methylation promoter. Our findings revealed role ELF3/MUC16 axis NPC, providing potential therapeutic targets for

Language: Английский

Citations

0