Targeting cholesterol biosynthesis promotes anti-tumor immunity by inhibiting long noncoding RNA SNHG29-mediated YAP activation

• Published in: Molecular therapy Vol. 29; no. 10; pp. 2995 - 3010
• Main Authors: Ni, Wen, Mo, Hui, Liu, Yuanyuan, Xu, Yuanyuan, Qin, Chao, Zhou, Yunxia, Li, Yuhui, Li, Yuqing, Zhou, Aijun, Yao, Su, Zhou, Rong, Huo, Jianping, Che, Liheng, Li, Jianming
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 06.10.2021; American Society of Gene & Cell Therapy
• Subjects: Adult; Aged; Aged, 80 and over; Animals; B7-H1 Antigen - genetics; B7-H1 Antigen - metabolism; Cell Line, Tumor; Cholesterol - biosynthesis; colorectal cancer; Colorectal Neoplasms - drug therapy; Colorectal Neoplasms - genetics; Colorectal Neoplasms - metabolism; Female; Gene Expression Regulation, Neoplastic - drug effects; HCT116 Cells; HT29 Cells; Humans; Hydroxymethylglutaryl CoA Reductases - metabolism; immune-checkpoint PD-L1; immunotherapy; lncRNA SNHG29; Male; Mice; Middle Aged; Original; Phosphorylation - drug effects; RNA, Long Noncoding - genetics; Signal Transduction - drug effects; simvastatin; Simvastatin - administration & dosage; Simvastatin - pharmacology; Tumor Microenvironment - drug effects; Ubiquitination - drug effects; Xenograft Model Antitumor Assays; YAP activation; YAP-Signaling Proteins - genetics; YAP-Signaling Proteins - metabolism; simvastatin; lncRNA SNHG29; YAP activation; colorectal cancer; immune-checkpoint PD-L1; immunotherapy

Anti-tumor immunity through checkpoint inhibitors, specifically anti-programmed death 1 (PD-1)/programmed death ligand 1 (PD-L1) interaction, is a promising approach for cancer therapy. However, as early clinical trials indicate that colorectal cancers (CRCs) do not respond well to immune-checkpoint...