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牙龈卟啉单胞菌通过 TGFβ 依赖性 Smad/YAP/TAZ 信号促进食管鳞癌的进展。

Porphyromonas gingivalis promotes progression of esophageal squamous cell cancer via TGFβ-dependent Smad/YAP/TAZ signaling.

机构信息

Henan Key Laboratory of Cancer Epigenetics, Cancer Hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and Technology, Luoyang, P. R. China.

Joint National Laboratory for Antibody Drug Engineering, Medical College of Henan University, Kaifeng, P. R. China.

出版信息

PLoS Biol. 2020 Sep 4;18(9):e3000825. doi: 10.1371/journal.pbio.3000825. eCollection 2020 Sep.

DOI:10.1371/journal.pbio.3000825
PMID:32886690
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7498034/
Abstract

Microbial dysbiosis in the upper digestive tract is linked to an increased risk of esophageal squamous cell carcinoma (ESCC). Overabundance of Porphyromonas gingivalis is associated with shorter survival of ESCC patients. We investigated the molecular mechanisms driving aggressive progression of ESCC by P. gingivalis. Intracellular invasion of P. gingivalis potentiated proliferation, migration, invasion, and metastasis abilities of ESCC cells via transforming growth factor-β (TGFβ)-dependent Drosophila mothers against decapentaplegic homologs (Smads)/Yes-associated protein (YAP)/Transcriptional coactivator with PDZ-binding motif (TAZ) activation. Smads/YAP/TAZ/TEA domain transcription factor1 (TEAD1) complex formation was essential to initiate downstream target gene expression, inducing an epithelial-mesenchymal transition (EMT) and stemness features. Furthermore, P. gingivalis augmented secretion and bioactivity of TGFβ through glycoprotein A repetitions predominant (GARP) up-regulation. Accordingly, disruption of either the GARP/TGFβ axis or its activated Smads/YAP/TAZ complex abrogated the tumor-promoting role of P. gingivalis. P. gingivalis signature genes based on its activated effector molecules can efficiently distinguish ESCC patients into low- and high-risk groups. Targeting P. gingivalis or its activated effectors may provide novel insights into clinical management of ESCC.

摘要

上消化道微生物失调与食管鳞状细胞癌（ESCC）风险增加有关。牙龈卟啉单胞菌的过度生长与 ESCC 患者的生存率降低有关。我们通过牙龈卟啉单胞菌研究了驱动 ESCC 侵袭性进展的分子机制。牙龈卟啉单胞菌的细胞内入侵通过转化生长因子-β（TGFβ）依赖性果蝇母体对抗 decapentaplegic 同源物（Smads）/Yes 相关蛋白（YAP）/转录共激活因子与 PDZ 结合基序（TAZ）激活增强了 ESCC 细胞的增殖、迁移、侵袭和转移能力。Smads/YAP/TAZ/TEA 结构域转录因子 1（TEAD1）复合物的形成对于启动下游靶基因表达至关重要，诱导上皮-间充质转化（EMT）和干细胞特征。此外，牙龈卟啉单胞菌通过糖蛋白 A 重复为主（GARP）上调增强了 TGFβ的分泌和生物活性。因此，破坏 GARP/TGFβ 轴或其激活的 Smads/YAP/TAZ 复合物均可消除牙龈卟啉单胞菌的促肿瘤作用。基于其激活效应分子的牙龈卟啉单胞菌特征基因可以有效地将 ESCC 患者分为低风险和高风险组。靶向牙龈卟啉单胞菌或其激活的效应物可能为 ESCC 的临床管理提供新的思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a760/7498034/ff624ce21a84/pbio.3000825.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a760/7498034/abaf2f505c87/pbio.3000825.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a760/7498034/397b84506536/pbio.3000825.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a760/7498034/cec6bdf6abdb/pbio.3000825.g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a760/7498034/ff624ce21a84/pbio.3000825.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a760/7498034/abaf2f505c87/pbio.3000825.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a760/7498034/397b84506536/pbio.3000825.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a760/7498034/cec6bdf6abdb/pbio.3000825.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a760/7498034/686b706a5c34/pbio.3000825.g004.jpg
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