Liu Jun, Yuan Jun-Fang, Wang Yu-Zhong
The Second Affiliated Hospital, Department of Urology, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, PR China.
Department of Endocrinology, Affiliated Hospital of Hebei University of Engineering, Handan, 056004, Hebei Province, PR China.
Exp Cell Res. 2022 Jul 1;416(1):113149. doi: 10.1016/j.yexcr.2022.113149. Epub 2022 Apr 9.
Long non-coding RNAs (lncRNAs) have emerged as novel players in cancer metabolism. lncRNA small nucleolar RNA host gene 7 (SNHG7) plays an oncogenic role in prostate cancer (PCa). However, the role and mechanism of SNHG7 in PCa metabolism remain largely undefined.
A cohort of 30 PCa tumors and their counterparts were collected. qRT-PCR was employed to detect target gene expression and RNA stability. CCK-8 assay was used to assess cell viability. N-methyladenosine (mA) level was measured by a commercial kit. Cell glycolysis was evaluated by measuring glucose uptake, lactate, ATP production and Extracellular acidification rate (ECAR). Bioinformatics analysis and RNA immunoprecipitation (RIP) assay were used to verify the interactions among SNHG7, serine/arginine-rich splicing factor 1 (SRSF1) and c-Myc.
SNHG7 and c-Myc were highly expressed in PCa tissues and cells. Methyltransferase-like 3 (METTL3)-mediated mA modification of SNHG7 and enhanced its stability. Silencing of SNHG7 suppressed proliferation and glycolysis in PCa cells. Mechanistically, SNHG7 regulated c-Myc via interacting with SRSF1. Gain- and loss-of function experiments revealed that SNHG7 promoted glycolysis via SRSF1/c-Myc axis in PC-3 and DU-145 cells.
METTL3-stabilized lncRNA SNHG7 accelerates glycolysis in PCa via SRSF1/c-Myc axis and inspires the understanding of mA roles in lncRNA metabolism and tumor progression.
长链非编码RNA（lncRNAs）已成为癌症代谢中的新角色。lncRNA小核仁RNA宿主基因7（SNHG7）在前列腺癌（PCa）中发挥致癌作用。然而，SNHG7在PCa代谢中的作用和机制仍 largely 未明确。
收集30例PCa肿瘤及其配对组织。采用qRT-PCR检测靶基因表达和RNA稳定性。使用CCK-8法评估细胞活力。通过商业试剂盒测量N-甲基腺苷（mA）水平。通过测量葡萄糖摄取、乳酸、ATP产生和细胞外酸化率（ECAR）评估细胞糖酵解。使用生物信息学分析和RNA免疫沉淀（RIP）试验验证SNHG7、富含丝氨酸/精氨酸的剪接因子1（SRSF1）和c-Myc之间的相互作用。
SNHG7和c-Myc在PCa组织和细胞中高表达。甲基转移酶样3（METTL3）介导的SNHG7的mA修饰增强了其稳定性。沉默SNHG7抑制了PCa细胞的增殖和糖酵解。机制上，SNHG7通过与SRSF1相互作用调节c-Myc。功能获得和丧失实验表明，SNHG7在PC-3和DU-145细胞中通过SRSF1/c-Myc轴促进糖酵解。
METTL3稳定的lncRNA SNHG7通过SRSF1/c-Myc轴加速PCa中的糖酵解，并促进对mA在lncRNA代谢和肿瘤进展中的作用的理解。
