LECT 2 Antagonizes FOXM1 Signaling via Inhibiting MET to Retard PDAC Progression

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers with minimally effective treatments, highlighting the importance of developing novel biomarkers and therapeutic targets. Here, we disclosed the mechanisms that leukocyte cell-derived chemotaxin-2 (LECT2) modulates PDAC develop...

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Published inFrontiers in cell and developmental biology Vol. 9; p. 661122
Main Authors Li, Xin, Lin, Pingping, Tao, Ye, Jiang, Xin, Li, Ting, Wang, Yunshan, Wang, Chenjing, Cao, Yu
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 15.04.2021
Subjects
Cell and Developmental Biology
FOXM1 signaling
HGF/MET
LECT2
PDAC
tumor growth
tumor growth
FOXM1 signaling
PDAC
HGF/MET
LECT2
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Summary:Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers with minimally effective treatments, highlighting the importance of developing novel biomarkers and therapeutic targets. Here, we disclosed the mechanisms that leukocyte cell-derived chemotaxin-2 (LECT2) modulates PDAC development using in vitro and in vivo models. LECT2 is downregulated in metastatic PDACs compared with the primary tumor, and its expression is correlated with multiple clinical pathologic features and prognosis. The absence promotes multiple malignant behaviors, including cell proliferation, epithelial-mesenchymal transition, migration, and invasion. In vivo studies showed that LECT2 overexpression inhibits tumor growth and lung metastasis. Mechanistically, LECT2 inhibits FOXM1 signaling by targeting HGF/MET to retard PDAC progression, revealing LECT2 as a promising biomarker and therapeutic target for PDAC in the future.
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Edited by: Ira Ida Skvortsova, Innsbruck Medical University, Austria
These authors have contributed equally to this work
Reviewed by: Guoxiong Zhou, Affiliated Hospital of Nantong University, China; Kuirong Jiang, Nanjing Medical University, China; Rui Kong, First Affiliated Hospital of Harbin Medical University, China
This article was submitted to Molecular and Cellular Oncology, a section of the journal Frontiers in Cell and Developmental Biology
ISSN:2296-634X
2296-634X
DOI:10.3389/fcell.2021.661122