The novel prognostic risk factor STC2 can regulate the occurrence and progression of osteosarcoma via the glycolytic pathway
The novel prognostic risk factor STC2 can regulate the occurrence and progression of osteosarcoma via the glycolytic pathway
复制标题
DOI：
10.1016/j.bbrc.2021.03.067
复制
发表时间：
2021-03-25
影响因子：
3.1
通讯作者：
Lv, Xiao-Bin
中科院分区：
文献类型：
--
作者：
Yu, Bo;Zhang, Feifei;Lv, Xiao-Bin
骨肉瘤是一种高度侵袭性的骨恶性肿瘤，通常发生在儿童和年轻人中。然而，尽管近年来骨肉瘤的临床治疗取得了相当大的成就，但骨肉瘤患者的总体生存率并未得到明显改善。癌细胞优先使用糖酵解而不是氧化磷酸化来满足其增加的能量和生物合成需求，这种现象称为瓦尔堡效应。糖酵解是多种癌症的驱动因素，并且正在成为一种新的癌症靶向治疗。在本研究中，我们建立了一个模型来筛选骨肉瘤中糖酵解相关基因。该模型的风险评分与骨肉瘤患者的临床特征相关。此外，功能测定发现 STC2 增强骨肉瘤细胞的糖酵解。 STC2 的调节会改变骨肉瘤中的葡萄糖消耗和乳酸产生以及 GLUT1 表达。此外，我们发现STC2表达水平的变化影响骨肉瘤细胞的增殖、侵袭和迁移。我们的研究结果表明，STC2 通过增强糖酵解而成为骨肉瘤细胞的新肿瘤促进因子。 ？ 2021 Elsevier Inc. 保留所有权利。
Osteosarcoma, a highly aggressive malignant tumor of the bone, usually occurs in children and young adults. However, although the considerable achievement in the clinical treatment of osteosarcoma recent years, the overall survival of osteosarcoma patients has not been obviously improved. Cancer cells preferentially use glycolysis instead of oxidative phosphorylation to meet their increased energetic and biosynthetic demands, a phenomenon known as the Warburg effect. Glycolysis is a driving factor in multiple cancers and is emerging as a new cancer target treatment. In the present study, we established a model to screen for glycolysis-associated genes in osteosarcoma. This risk score of the model were correlated with clinical characteristics osteosarcoma patients. Besides, a functional assay identified that STC2 enhanced the glycolysis of osteosarcoma cells. Modulation of STC2 changes glucose consumption and lactate production as well as GLUT1 expression in osteosarcoma. Furthermore, we identified that change in the expression levels of STC2 affected the proliferation, invasion, and migration of osteosarcoma cells. Our findings showed STC2 as a new tumor-promoting factor of osteosarcoma cells through enhancing glycolysis. ? 2021 Elsevier Inc. All rights reserved.