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.
journal_name
PLoS Bioljournal_title
PLoS biologyauthors
Qi YJ,Jiao YL,Chen P,Kong JY,Gu BL,Liu K,Feng DD,Zhu YF,Ruan HJ,Lan ZJ,Liu QW,Mi YJ,Guo XQ,Wang M,Liang GF,Lamont RJ,Wang H,Zhou FY,Feng XS,Gao SGdoi
10.1371/journal.pbio.3000825subject
Has Abstractpub_date
2020-09-04 00:00:00pages
e3000825issue
9eissn
1544-9173issn
1545-7885pii
PBIOLOGY-D-20-00010journal_volume
18pub_type
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