PGRP-S通过与TTC1相互作用，经由丝裂原活化蛋白激酶/细胞外信号调节激酶（MAPK/ERK）信号通路促进肝细胞癌进展。
PGRP-S promotes hepatocellular carcinoma progression via MAPK/ERK pathway by interaction with TTC1.
作者信息
Zhu Huifang, Feng Shuang, Lv Sizhen, Zhao Di, Chang Xuanhe, Fan Shangqian, Wang Xia, Qian Xinlai
机构信息
Department of Pathology, The Third Affiliated Hospital of Xinxiang Medical University, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, Henan, China.
The First Bethune Clinical Medical College of Ji Lin University, Changchun, Jilin, China.
出版信息
Sci Rep. 2025 Aug 4;15(1):28367. doi: 10.1038/s41598-025-12160-x.
Abnormal expression of PGRP-S plays an important role in the development and progression of hepatocellular carcinoma (HCC), although the mechanism has remained elusive. In this study, we aimed to investigate the biological function and potential mechanism of PGRP-S in HCC. We found that PGRP-S was upregulated in HCC tissues compared to adjacent tissues. The increased expression of PGRP-S correlated with the differentiation and lymph node metastasis of HCC. PGRP-S obviously promoted HCC cell proliferation, migration and invasion in vitro. In vivo nude mouse models showed that PGRP-S enhanced tumor growth and pulmonary metastasis. Mechanistically, PGRP-S interacted with TTC1 and activated MAPK/ERK pathway, leading to HCC cell proliferation, migration and invasion. Therfore, our conclusion is PGRP-S promotes HCC cell proliferation, migration and invasion by activating MAPK/ERK pathway, which provides a new potential strategy for HCC treatment by targeting PGRP-S-TTC1 axis.
尽管机制尚不清楚，但肽聚糖识别蛋白-S（PGRP-S）的异常表达在肝细胞癌（HCC）的发生和发展中起重要作用。在本研究中，我们旨在探讨PGRP-S在HCC中的生物学功能和潜在机制。我们发现，与癌旁组织相比，PGRP-S在HCC组织中上调。PGRP-S表达增加与HCC的分化和淋巴结转移相关。PGRP-S在体外明显促进HCC细胞增殖、迁移和侵袭。体内裸鼠模型显示，PGRP-S增强肿瘤生长和肺转移。机制上，PGRP-S与TTC1相互作用并激活MAPK/ERK通路，导致HCC细胞增殖、迁移和侵袭。因此，我们的结论是PGRP-S通过激活MAPK/ERK通路促进HCC细胞增殖、迁移和侵袭，这为通过靶向PGRP-S-TTC1轴治疗HCC提供了一种新的潜在策略。
Zotero 插件