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血小板与肿瘤细胞的直接相互作用通过激活 TLR4/ADAM10/CX3CL1 轴加剧肝癌转移。

Direct interaction of platelet with tumor cell aggravates hepatocellular carcinoma metastasis by activating TLR4/ADAM10/CX3CL1 axis.

机构信息

Department of Pharmacology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.

Department of Anatomy, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan, China.

出版信息

Cancer Lett. 2024 Mar 31;585:216674. doi: 10.1016/j.canlet.2024.216674. Epub 2024 Jan 25.

Abstract

Metastasis is the main culprit of cancer-related death and account for the poor prognosis of hepatocellular carcinoma. Although platelets have been shown to accelerate tumor cell metastasis, the exact mechanism remained to be fully understood. Here, we found that high blood platelet counts and increased tumor tissue ADAM10 expression indicated the poor prognosis of HCC patients. Meanwhile, blood platelet count has positive correlation with tumor tissue ADAM10 expression. In vitro, we revealed that platelet increased ADAM10 expression in tumor cell through TLR4/NF-κB signaling pathway. ADAM10 catalyzed the shedding of CX3CL1 which bound to CX3CR1 receptor, followed by inducing epithelial to mesenchymal transition and activating RhoA signaling in cancer cells. Moreover, knockdown HCC cell TLR4 (Tlr4) or inhibition of ADAM10 prevented platelet-increased tumor cell migration, invasion and endothelial permeability. In vivo, we further verified in mice lung metastatic model that platelet accelerated tumor metastasis via cancer cell TLR4/ADAM10/CX3CL1 axis. Overall, our study provides new insights into the underlying mechanism of platelet-induced HCC metastasis. Therefore, targeting the TLR4/ADAM10/CX3CL1 axis in cancer cells hold promise for the inhibition of platelet-promoted lung metastasis of HCC.

摘要

转移是癌症相关死亡的主要罪魁祸首,也是肝细胞癌预后不良的原因。尽管已有研究表明血小板可加速肿瘤细胞转移,但确切机制仍有待充分阐明。在这里,我们发现高血小板计数和肿瘤组织 ADAM10 表达增加预示着 HCC 患者的预后不良。同时,血小板计数与肿瘤组织 ADAM10 表达呈正相关。在体外,我们揭示了血小板通过 TLR4/NF-κB 信号通路增加肿瘤细胞中 ADAM10 的表达。ADAM10 催化 CX3CL1 的脱落,后者与 CX3CR1 受体结合,随后诱导癌细胞发生上皮间质转化并激活 RhoA 信号通路。此外,敲低 HCC 细胞 TLR4(Tlr4)或抑制 ADAM10 可阻止血小板增加肿瘤细胞的迁移、侵袭和内皮通透性。在体内,我们在小鼠肺转移模型中进一步证实,血小板通过癌细胞 TLR4/ADAM10/CX3CL1 轴加速肿瘤转移。总之,我们的研究为血小板诱导 HCC 转移的潜在机制提供了新的见解。因此,靶向癌细胞中的 TLR4/ADAM10/CX3CL1 轴有望抑制血小板促进的 HCC 肺转移。

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