CCN6 as a profibrotic mediator that stimulates the proliferation of lung fibroblasts via the integrin .BETA.1/focal adhesion kinase pathway

Batmunkh, Rentsenkhand; Nishioka, Yasuhiko; Aono, Yoshinori; Azuma, Momoyo; Kinoshita, Katsuhiro; Kishi, Jun; Makino, Hideki; Kishi, Masami; Takezaki, Akio; Sone, Saburo

doi:10.2152/jmi.58.188

Cited by 17 publications

(14 citation statements)

References 38 publications

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“…CCN1 is also expressed during wound healing and development of fibrosis; however, this molecule appears to terminate these processes by inducing senescence in myofibroblasts through a DNA damage response pathway and ROS formation [5,80,81]. In this context, one may not overlook the possible involvement of CCN4 and CCN6 as well [11,82]. In this context, one may not overlook the possible involvement of CCN4 and CCN6 as well [11,82].…”

Section: Inflammation Wound Healing and Fibrosismentioning

confidence: 99%

Cellular and molecular actions of CCN2/CTGF and its role under physiological and pathological conditions

2014

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CCN family protein 2 (CCN2), also widely known as connective tissue growth factor (CTGF), is one of the founding members of the CCN family of matricellular proteins. Extensive investigation on CCN2 over decades has revealed the novel molecular action and functional properties of this unique signalling modulator. By its interaction with multiple molecular counterparts, CCN2 yields highly diverse and context-dependent biological outcomes in a variety of microenvironments. Nowadays, CCN2 is recognized to conduct the harmonized development of relevant tissues, such as cartilage and bone, in the skeletal system, by manipulating extracellular signalling molecules involved therein by acting as a hub through a web. However, on the other hand, CCN2 occasionally plays profound roles in major human biological disorders, including fibrosis and malignancies in major organs and tissues, by modulating the actions of key molecules involved in these clinical entities. In this review, the physiological and pathological roles of this unique protein are comprehensively summarized from a molecular network-based viewpoint of CCN2 functionalities.

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Section: Inflammation Wound Healing and Fibrosismentioning

confidence: 99%

Cellular and molecular actions of CCN2/CTGF and its role under physiological and pathological conditions

2014

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“…Lung fibrosis can be induced by a number of endogenous and exogenous factors including iatrogenic ones. Interestingly, CCN6 was found to be induced in a pulmonary fibrosis model of mice treated with bleomycin (126). Subsequent investigation in vitro revealed relatively weak fibrogenic activity of CCN6.…”

Section: The Ccn Family In Biological Responses and Diseases Fibrosismentioning

confidence: 99%

“…Subsequent investigation in vitro revealed relatively weak fibrogenic activity of CCN6. Although further study to verify its biological significance is necessary, CCN6 may also join the CCN family network for fibrosis regulation as a profibrotic member (126).…”

Section: The Ccn Family In Biological Responses and Diseases Fibrosismentioning

confidence: 99%

The CCN family acting throughout the body: recent research developments

Kubota

Takigawa

2013

BioMolecular Concepts

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The animal body is composed of a variety of cells and extracellular matrices that are organized and orchestrated in a harmonized manner to support life. Therefore, the critical importance of a comprehensive understanding of the molecular network surrounding and integrating the cells is now emphasized. The CCN family is a novel group of matricellular proteins that interact with and orchestrate a number of extracellular signaling and matrix molecules to construct and maintain living tissues. This family comprises six distinct members in mammals, which are characterized by a unique and conserved modular structure. These proteins are not targeted to limited and specific receptors to execute specific missions, but manipulate a vast number of biomolecules in the network by serving as a molecular hub at the center. The unified nomenclature, CCN, originates from a simple acronym of the three classical members, which helps us to avoid having any preconception about their pleiotropic and anonymous functional nature. In this review, after a brief summary of the general molecular concepts regarding the CCN family, new aspects of each member uncovered by recent research are introduced, which represent, nevertheless, only the tip of the iceberg of the profound functionality of these molecules.

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“…9 Members of CCN family are involved in many vital biological functions, including cell proliferation, adhesion, angiogenesis, ECM production, migration, tumour growth and wound healing, 10 and dysregulation of this family contributed to the tumorigenicity of various tumours. [14][15][16] Moreover, it was reported that β-catenin dysregulation was partially correlated with inactivating mutations in WISP3 gene in metaplastic carcinomas of the breast. [14][15][16] Moreover, it was reported that β-catenin dysregulation was partially correlated with inactivating mutations in WISP3 gene in metaplastic carcinomas of the breast.…”

Section: Introductionmentioning

confidence: 99%

Liver cancer: WISP3 suppresses hepatocellular carcinoma progression by negative regulation of β‐catenin/TCF/LEF signalling

et al. 2019

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Objectives: Wnt1-inducible signalling pathway protein 3 (WISP3/CCN6) belongs to the CCN (CYR61/CTGF/NOV) family of proteins, dysregulation of this family contributed to the tumorigenicity of various tumours. In this study, we need to explore its role in hepatocellular carcinoma that remains largely elusive. Materials and Methods:The expression of WISP3/CCN6 was analysed by qRT-PCR and Western blotting. Effects of WISP3 on proliferation and metastasis of HCC cells were examined, respectively, by MTT assay and Boyden Chamber. Roles of WISP3 on HCC tumour growth and metastatic ability in vivo were detected in nude mice.Related mechanism study was confirmed by immunofluorescence and Western blotting. Results: The expression of WISP3 was significantly downregulated in HCC clinical samples and cell lines, and reversely correlated with the tumour size. Forced expression of WISP3 in HCC cells significantly suppressed cell growth and migration in vitro as well as tumour growth and metastatic seeding in vivo. In contrast, downregulation of WISP3 accelerated cell proliferation and migration, and promoted in vivo S U PP O RTI N G I N FO R M ATI O N Additional supporting information may be found online in the Supporting Information section at the end of the article.

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CCN6 as a profibrotic mediator that stimulates the proliferation of lung fibroblasts via the integrin .BETA.1/focal adhesion kinase pathway

Cited by 17 publications

References 38 publications

Cellular and molecular actions of CCN2/CTGF and its role under physiological and pathological conditions

Cellular and molecular actions of CCN2/CTGF and its role under physiological and pathological conditions

The CCN family acting throughout the body: recent research developments

Liver cancer: WISP3 suppresses hepatocellular carcinoma progression by negative regulation of β‐catenin/TCF/LEF signalling

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