代谢重编程是肿瘤进展的一个重要特征。长链非编码RNA（lncRNA）小核RNA载体基因6（SNHG6）在肝细胞癌（HCC）中作为原癌基因发挥作用，但其在糖酵解方面的作用大多未知。通过葡萄糖摄取、乳酸产生、氧气消耗率（OCR）和细胞外酸化率（ECAR）以及糖酵解酶水平来评估SNHG6和增殖阻滞1（BOP1）在糖酵解中的作用。通过Western blotting、MS2 pull-down、RNA pull-down和RIP assay确认SNHG6对BOP1蛋白的调节作用。HCC组织和细胞中SNHG6和BOP1水平升高。SNHG6和BOP1是HCC患者的预后因子，与TP53突变和肿瘤分级显著相关。SNHG6促进了HCC细胞系的增殖，抑制了凋亡，增强了葡萄糖摄取和乳酸产生，减少了OCR，并增加了ECAR。SNHG6能够结合BOP1蛋白并增强其稳定性。BOP1过表达可挽救HCCLM3和SMMC-7721细胞中增殖、凋亡和糖酵解的变化。我们的数据表明，SNHG6通过结合BOP1蛋白并增强其稳定性，加速HCC细胞系的增殖和糖酵解，抑制凋亡。SNHG6和BOP1均是HCC的有前途的预后和治疗标志物。© 2022作者。由Informa UK Limited出版，交易Taylor＆Francis Group。

Metabolic reprogramming is an important feature in tumor progression. Long noncoding RNA's (lncRNA) small nucleolar RNA host gene 6 (SNHG6) acts as a proto-oncogene in hepatocellular carcinoma (HCC) but its role in glycolysis is mostly unknown. The role of SNHG6 and Block of proliferation 1 (BOP1) on glycolysis is assessed by glucose uptake, lactate production, oxygen consumptive rate (OCR) and extracellular acidification rate (ECAR) and glycolytic enzyme levels. The regulatory effect of SNHG6 on BOP1 protein was confirmed by Western blotting, MS2 pull-down, RNA pull-down, and RIP assay. SNHG6 and BOP1 levels were increased in HCC tissues and cells. SNHG6 and BOP1 were prognostic factors in HCC patients and significantly correlated to TP53 mutant and tumor grade. SNHG6 promoted proliferation, inhibited apoptosis, enhanced glucose uptake and lactate production, decreased OCR, and increased ECAR in HCC cell lines. SNHG6 could bind the BOP1 protein and enhance its stability. BOP1 overexpression rescued the change of proliferation, apoptosis, and glycolysis in HCCLM3 and SMMC-7721 cells. Our data indicate that SNHG6 accelerates proliferation and glycolysis and inhibits the apoptosis of HCC cell lines by binding the BOP1 protein and enhancing its stability. Both SNHG6 and BOP1 are promising prognostic and therapeutic markers in HCC.© 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.