Translational Research Institute, Jinan University, Guangzhou, 510632, Guangdong, China.
MOE Key Laboratory of Tumor Molecular Biology, Department of Pharmacology, Clinical Translational Center for Targeted Drug, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Mol Cell Biochem. 2021 Sep;476(9):3423-3431. doi: 10.1007/s11010-021-04171-9. Epub 2021 May 10.
Reprogramming of energy metabolism is a hallmark of cancer which is prevalent worldwide. Octamer transcription factor-1 (OCT1) is a well-known transcription factor. However, the role of OCT1 in metabolism remodeling has not been well defined. In the present study, we found that OCT1 was up-regulated in non-small cell lung cancer (NSCLC) and correlated with poor patient survival. Further data identified that OCT1 increased glycolysis flux, promoting proliferation in lung cancer cells. Mechanistically, OCT1 facilitated the aerobic glycolysis and cell proliferation via up-regulation of hexokinase 2 (HK2), a crucial enzyme of the Warburg effect. Hence, our findings indicate that, in NSCLC, high levels of OCT1 contribute to the Warburg effect through up-regulation of HK2, linking up the OCT1/HK2 axis and cancer progression, which provide a potential biomarker and therapeutic target for NSCLC treatment.
能量代谢重编程是一种在全球范围内普遍存在的癌症特征。八聚体转录因子-1（OCT1）是一种众所周知的转录因子。然而，OCT1 在代谢重塑中的作用尚未得到很好的定义。在本研究中，我们发现 OCT1 在非小细胞肺癌（NSCLC）中上调，并与患者预后不良相关。进一步的数据表明，OCT1 通过增加糖酵解通量促进肺癌细胞的增殖。机制上，OCT1 通过上调己糖激酶 2（HK2）促进有氧糖酵解和细胞增殖，HK2 是瓦博格效应的关键酶。因此，我们的研究结果表明，在 NSCLC 中，高水平的 OCT1 通过上调 HK2 促进瓦博格效应，连接 OCT1/HK2 轴和癌症进展，为 NSCLC 的治疗提供了一个潜在的生物标志物和治疗靶点。
