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LMO2 可减弱肺癌和乳腺癌肿瘤微环境中的糖酵解代谢,并促进细胞毒性 T 淋巴细胞浸润。

LMO2 attenuates glycolytic metabolism and facilitates cytotoxic T-lymphocyte infiltration in the tumor environment of lung and breast cancers.

机构信息

School of Medicine, Nankai University, Tianjin, China.

School of Medicine, Nankai University, Tianjin, China.

出版信息

Biochem Biophys Res Commun. 2023 Oct 1;675:170-176. doi: 10.1016/j.bbrc.2023.07.024. Epub 2023 Jul 18.

Abstract

Aerobic glycolysis preferentially exists in many cancer cells. LMO2 is an adaptor protein ubiquitously expressed in many epithelia and their malignancies, and it mediates broad-spectrum protein interactions. In this study, results showed that LMO2 directly interacted with glycolytic enzymes PGK1, PGAM1 and LDHA/LDHB, attenuated the glycolytic metabolism flow characterized by decreased glucose intake, ATP production and lactic acid excretion in lung and breast cancer cells, and was positively associated with of CD8 T-lymphocyte infiltration in the tumor microenvironment. These findings reveal a novel role of LMO2 on modulating glycolysis in tumor cells and cytotoxic T-lymphocyte infiltration in the tumor microenvironment, which expands our knowledge of LMO2 in the field of solid tumors.

摘要

有氧糖酵解优先存在于许多癌细胞中。LMO2 是一种在许多上皮细胞及其恶性肿瘤中广泛表达的衔接蛋白,它介导广谱的蛋白质相互作用。在这项研究中,结果表明 LMO2 直接与糖酵解酶 PGK1、PGAM1 和 LDHA/LDHB 相互作用,减弱了肺癌和乳腺癌细胞中以葡萄糖摄取、ATP 产生和乳酸排泄减少为特征的糖酵解代谢流,并且与肿瘤微环境中 CD8 T 淋巴细胞浸润呈正相关。这些发现揭示了 LMO2 在调节肿瘤细胞糖酵解和肿瘤微环境中细胞毒性 T 淋巴细胞浸润中的新作用,这扩展了我们对 LMO2 在实体肿瘤领域的认识。

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