肾细胞癌
血管生成拟态
表观遗传学
肺癌
癌症研究
癌症
肾透明细胞癌
去甲基化
生物
DNA甲基化
血管生成
化学
病理
新生血管
免疫组织化学
肾
医学
转移
生物化学
基因表达
基因
遗传学
作者
Huan Wang,Li-Ya Wang,Qiming Zheng,Zeyi Lu,Yuanlei Chen,Danyang Shen,Dingwei Xue,Minxiao Jiang,Lifeng Ding,Jie Zhang,Haiyang Wu,Xia Liqun,Jun Qian,Gonghui Li,Jieyang Lu
摘要
Metabolism reprograming is a hallmark of cancer and plays an important role in tumor progression. The aberrant metabolism in renal cell carcinoma (RCC) leads to accumulation of the oncometabolite L-2-hydroxyglurate (L-2HG). L-2HG has been reported to inhibit the activity of some α-ketoglutarate-dependent dioxygenases such as TET enzymes, which mediate epigenetic alteration, including DNA and histone demethylation. However, the detailed functions of L-2HG in renal cell carcinoma have not been investigated thoroughly. In our study, we found that L-2HG was significantly elevated in tumor tissues compared to adjacent tissues. Furthermore, we demonstrated that L-2HG promoted vasculogenic mimicry (VM) in renal cancer cell lines through reducing the expression of PHLDB2. A mechanism study revealed that activation of the ERK1/2 pathway was involved in L-2HG-induced VM formation. In conclusion, these findings highlighted the pathogenic link between L-2HG and VM and suggested a novel therapeutic target for RCC.
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