Periostin Promotes Colorectal Tumorigenesis through Integrin-FAK-Src Pathway-Mediated YAP/TAZ Activation

Ma, Handong; Wang, Jing; Zhao, Xueqin; Wu, Tiantian; Huang, Zhengjie; Chen, Dafan; Liu, Yingfu; Ouyang, Gaoliang

doi:10.1016/j.celrep.2019.12.075

Cited by 129 publications

(119 citation statements)

References 47 publications

(60 reference statements)

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“…A previous study described that a mutant cell line lacking YAP showed decreased Thbs1 levels along with down-regulation of YAP target genes and FA molecules, indicating that Thbs1 may act as a feedforward driver for YAP signaling (41). Interestingly, the proteolytic remodeling of laminin-1 has been shown to modulate awakening of dormant cancer cells through integrin/FAK/ERK/MLCK (myosin lightchain kinase)/YAP signaling (42), and fibroblast-derived periostin (encoded by Postn) has been shown to mediate colorectal tumorigenesis through integrin/FAK/Src/YAP signaling (43), further supporting the idea that an ECM can regulate YAP signaling in various biological conditions.…”

Section: Discussionmentioning

confidence: 99%

Matrix mechanotransduction mediated by thrombospondin-1/integrin/YAP in the vascular remodeling

Yamashiro

Thang

Ramírez

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

110

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The extracellular matrix (ECM) initiates mechanical cues that activate intracellular signaling through matrix–cell interactions. In blood vessels, additional mechanical cues derived from the pulsatile blood flow and pressure play a pivotal role in homeostasis and disease development. Currently, the nature of the cues from the ECM and their interaction with the mechanical microenvironment in large blood vessels to maintain the integrity of the vessel wall are not fully understood. Here, we identified the matricellular protein thrombospondin-1 (Thbs1) as an extracellular mediator of matrix mechanotransduction that acts via integrin αvβ1 to establish focal adhesions and promotes nuclear shuttling of Yes-associated protein (YAP) in response to high strain of cyclic stretch. Thbs1-mediated YAP activation depends on the small GTPase Rap2 and Hippo pathway and is not influenced by alteration of actin fibers. Deletion of Thbs1 in mice inhibited Thbs1/integrin β1/YAP signaling, leading to maladaptive remodeling of the aorta in response to pressure overload and inhibition of neointima formation upon carotid artery ligation, exerting context-dependent effects on the vessel wall. We thus propose a mechanism of matrix mechanotransduction centered on Thbs1, connecting mechanical stimuli to YAP signaling during vascular remodeling in vivo.

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Section: Discussionmentioning

confidence: 99%

Matrix mechanotransduction mediated by thrombospondin-1/integrin/YAP in the vascular remodeling

Yamashiro

Thang

Ramírez

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

110

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“…Similarly, high expression of POSTN, also overrepresented in PUC-GBC2, might explain the higher migratory ability of these cells. POSTN encodes for periostin, a multifunctional ECM protein that contributes to the remodeling of the tumor microenvironment during tumor progression [36]. In CCA and hepatoblastoma, overexpressed periostin was found to induce cell migration and epithelial-to-mesenchymal transition (EMT) features [37,38].…”

Section: Discussionmentioning

confidence: 99%

Functional and genomic characterization of three novel cell lines derived from a metastatic gallbladder cancer tumor

et al. 2020

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Background: Gallbladder cancer (GBC) is the most common tumor of the biliary tract. The incidence of GBC shows a large geographic variability, being particularly frequent in Native American populations. In Chile, GBC represents the second cause of cancer-related death among women. We describe here the establishment of three novel cell lines derived from the ascitic fluid of a Chilean GBC patient, who presented 46% European, 36% Mapuche, 12% Aymara and 6% African ancestry.Results: After immunocytochemical staining of the primary cell culture, we isolated and comprehensively characterized three independent clones (PUC-GBC1, PUC-GBC2 and PUC-GBC3) by short tandem repeat DNA profiling and RNA sequencing as well as karyotype, doubling time, chemosensitivity, in vitro migration capability and in vivo tumorigenicity assay. Primary culture cells showed high expression of CK7, CK19, CA 19-9, MUC1 and MUC16, and negative expression of mesothelial markers. The three isolated clones displayed an epithelial phenotype and an abnormal structure and number of chromosomes. RNA sequencing confirmed the increased expression of cytokeratin and mucin genes, and also of TP53 and ERBB2 with some differences among the three cells lines, and revealed a novel exonic mutation in NF1. The PUC-GBC3 clone was the most aggressive according to histopathological features and the tumorigenic capacity in NSG mice. Conclusions:The first cell lines established from a Chilean GBC patient represent a new model for studying GBC in patients of Native American descent.

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“…In this regard, TGFbeta-activated CAFs may secrete POSTN in order to increase proliferation, motility, and invasive properties in head and neck cancer (HNC) cells (Qin et al, 2016). Similarly, CAF-secreted POSTN may also promote tumor progression in CRC through YAP/TAZ activation in cancer cells (Ma et al, 2020). Of note, Deng and colleagues showed that the YAP-activated Wnt/βcatenin pathway promotes colon tumorigenesis (Deng et al, 2018).…”

Section: Metastatic Cancer Cells Spreadingmentioning

confidence: 99%

Determinants and Functions of CAFs Secretome During Cancer Progression and Therapy

Linares

Marín-Jiménez

Badia-Ramentol

et al. 2021

Front. Cell Dev. Biol.

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Multiple lines of evidence are indicating that cancer development and malignant progression are not exclusively epithelial cancer cell-autonomous processes but may also depend on crosstalk with the surrounding tumor microenvironment (TME). Cancer-associated fibroblasts (CAFs) are abundantly represented in the TME and are continuously interacting with cancer cells. CAFs are regulating key mechanisms during progression to metastasis and response to treatment by enhancing cancer cells survival and aggressiveness. The latest advances in CAFs biology are pointing to CAFs-secreted factors as druggable targets and companion tools for cancer diagnosis and prognosis. Especially, extensive research conducted in the recent years has underscored the potential of several cytokines as actionable biomarkers that are currently evaluated in the clinical setting. In this review, we explore the current understanding of CAFs secretome determinants and functions to discuss their clinical implication in oncology.

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Periostin Promotes Colorectal Tumorigenesis through Integrin-FAK-Src Pathway-Mediated YAP/TAZ Activation

Cited by 129 publications

References 47 publications

Matrix mechanotransduction mediated by thrombospondin-1/integrin/YAP in the vascular remodeling

Matrix mechanotransduction mediated by thrombospondin-1/integrin/YAP in the vascular remodeling

Functional and genomic characterization of three novel cell lines derived from a metastatic gallbladder cancer tumor

Determinants and Functions of CAFs Secretome During Cancer Progression and Therapy

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