HS3ST1 通过靶向 SPOP/FADD/NF-κB 通路促进非小细胞肺癌进展。

HS3ST1 Promotes Non-Small-Cell Lung Cancer Progression by Targeting the SPOP/FADD/NF-B Pathway.

机构信息

Department of Oncology, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai 200433, China.

Department of Respiratory and Critical Care Medicine, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai 200433, China.

出版信息

Biomed Res Int. 2022 Jul 19;2022:5509346. doi: 10.1155/2022/5509346. eCollection 2022.

Heparan sulfate proteoglycan is a key component of cell microenvironment and plays an important role in cell-cell interaction, adhesion, migration, and signal transduction. Heparan sulfate 3-O-sulfotransferase 1 (HS3ST1) is a metabolic-related gene of HS. The present study was aimed at exploring the role of HS3ST1 in the progress of non-small-cell lung cancer (NSCLC). Our results illustrated that HS3ST1 promoted the malignant behaviors of NSCLC cells both and . HS3ST1 was found to inhibit spot-type zinc finger protein (SPOP) expression, which might inhibit the NF-B pathway activation through mediating the degradation of Fas-associated death domain protein (FADD). By analyzing NSCLC patient samples, we also found increased HS3ST1 expression and decreased SPOP expression in tumor tissues in contrast with those in adjoining normal tissues. In conclusion, HS3ST1 promotes NSCLC tumorigenesis by regulating SPOP/FADD/NF-B pathway.

硫酸乙酰肝素蛋白聚糖是细胞微环境的关键组成部分，在细胞-细胞相互作用、黏附、迁移和信号转导中发挥重要作用。硫酸乙酰肝素 3-O-磺基转移酶 1（HS3ST1）是 HS 的代谢相关基因。本研究旨在探讨 HS3ST1 在非小细胞肺癌（NSCLC）进展中的作用。我们的结果表明，HS3ST1 促进了 NSCLC 细胞的恶性行为。发现 HS3ST1 抑制点型锌指蛋白（SPOP）的表达，可能通过介导 Fas 相关死亡结构域蛋白（FADD）的降解来抑制 NF-B 途径的激活。通过分析 NSCLC 患者样本，我们还发现肿瘤组织中 HS3ST1 的表达增加，而相邻正常组织中 SPOP 的表达降低。总之，HS3ST1 通过调节 SPOP/FADD/NF-B 通路促进 NSCLC 肿瘤发生。