TGF-β1 and FAK Regulate Periostin Expression in PDL Fibroblasts

Wen, Weiyan; Chau, Eddy; Jackson-Boeters, Linda; Elliott, Christopher G.; Daley, Tom D.; Hamilton, David A.

doi:10.1177/0022034510378684

Cited by 72 publications

(67 citation statements)

References 22 publications

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“…TGF-β increased the expression of periostin, which has been previously shown in gingival and periodontal ligament fibroblasts [8]. However, the effect of TGF-β on periostin expression in tumours has been seldom studied.…”

Section: Discussionmentioning

confidence: 88%

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Periostin Mediates TGF-β-Induced Epithelial Mesenchymal Transition in Prostate Cancer Cells

Tong

Zhao

et al. 2015

Cell Physiol Biochem

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Background: In our previous study, we found that periostin was upregulated in prostate cancer, and its expression could be modulated by TGF-β. TGF-β could upregulate periostin expression in some cells, and both TGF-β and periostin could induce epithelial mesenchymal transition (EMT). We aimed to study the effect of periostin in the process of TGF-β-induced EMT in prostate cancer cells. Methods: We constructed a lentivirus vector containing the periostin gene and transduced it into PC3 and DU145 cells. After confirming periostin overexpression by PCR and Western blotting, we used an MTT assay to establish a growth curve to measure cell proliferation. Additionally, we performed transwell and wound healing assays to measure cell invasion and migration, respectively. Lastly, we measured the expression of EMT associated factors using Western blot analysis to test the effect of periostin on EMT in prostate cancer cells. Results: PCR and Western blot analyses confirmed that periostin was upregulated after infection with the periostin lentiviral vector. Periostin overexpression promoted increased cell proliferation, invasion, and migration as measured by MTT, transwell, and wound healing assays, respectively. Western blot analysis illustrated that periostin overexpression increased the expression of EMT associated factors, and periostin overexpression activated Akt and GSK-3β, which could be inhibited using a PI3K inhibitor. Additionally, TGF-β increased the levels of STAT3, Twist1 and periostin, while both STAT3 shRNA and Twist1 shRNA inhibited periostin expression. However, STAT3 shRNA also decreased Twist1 expression. Although reduction of STAT3, Twist1 or periostin levels with shRNA inhibited TGF-β-induced overexpression of EMT associated factors, periostin overexpression could reverse such inhibition by interfering with STAT3 and Twist1. Similarly, periostin overexpression also reversed inhibition of cell invasion induced by interference of STAT3 and Twist1. Conclusion: Our findings indicate that periostin is an important mediator of TGF-β-induced EMT and suggest that periostin is a potential therapeutic target for suppressing the metastatic progression of prostate cancer.

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Section: Discussionmentioning

confidence: 88%

“…It has been shown that periostin can induce EMT via the activation of the PI3K/Akt pathway in prostate cancer cells [6,7]. Additionally, it has been reported that TGF-β can modulate periostin expression in periodontal ligament and gingival fibroblasts [8]. However, similar studies in tumour cells are still lacking.…”

Section: Introductionmentioning

confidence: 99%

Periostin Mediates TGF-β-Induced Epithelial Mesenchymal Transition in Prostate Cancer Cells

Tong

Zhao

et al. 2015

Cell Physiol Biochem

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“…Adult periostin null mice were shown to exhibit a periodontal disease phenotype including external root resorption caused by collagen fibril disorganization with defective fibronectin expression (17,22). Additionally, it has been reported that TGF-β can increase periostin expression in PDL (27). In the present study, we evaluated the functional significance of TGF-β signaling on EMT and fragmentation in HERS cells, and suggested that the fragmented HERS cells played as PDL fibroblasts with periostin expression.…”

mentioning

confidence: 78%

<b>Hertwig’s epithelial root sheath cells contribute to formation of periodontal ligament through epithelial-mesenchymal transition by </b><b>TGF-β </b>

et al. 2017

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In tooth root development, periodontal ligament (PDL) and cementum are formed by the coordination with the fragmentation of Hertwig's epithelial root sheath (HERS) and the differentiation of dental follicle mesenchymal cells. However, the function of the dental epithelial cells after HERS fragmentation in the PDL is not fully understood. Here, we found that TGF-β regulated HERS fragmentation via epithelial-mesenchymal transition (EMT), and the fragmented epithelial cells differentiated into PDL fibroblastic cells with expressing of PDL extracellular matrix (ECM). In the histochemical analysis, TGF-β was expressed in odontoblast layer adjacent of HERS during root development. Periostin expression was detected around fragmented epithelial cells on the root surface, but not in HERS. In the experiment using an established mouse HERS cell line (HERS01a), TGF-β1 treatment decreased E-cadherin and relatively increased N-cadherin expression. TGF-β1 treatment in HERS01a induced further expression of important ECM proteins for acellular cementum and PDL development such as fibronectin and periostin. Taken together, activation of TGF-β signaling induces HERS fragmentation through EMT and the fragmented HERS cells contribute to formation of PDL and acellular cementum through periostin and fibronectin expression.

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“…In situ hybridization and immunohistochemistry showed that periostin is expressed in the PDL, in dental pulp at the sites of hard/soft tissue interfaces in mouse and human tooth [32,33]. Periostin is secreted by fibroblasts and osteoblasts in PDL.…”

Section: Periostin Is Expressed In Bone and Teethmentioning

confidence: 99%

“…TGF-β and BMP are well-known regulators of bone development by stimulating the differentiation of osteoblast progenitors [51,52]. TGF-β, BMP-2, activin, and retinoic acid all stimulate periostin expression in osteoblasts [3,28,33,53,54]. Blocking TGF-β receptor activation or the noncanonical focal adhesion kinase (FAK) pathway reduced periostin mRNA expression.…”

Section: Periostin Expression Is Regulated By Hormones and Growth Facmentioning

confidence: 99%

The multiple facets of periostin in bone metabolism

2012

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Periostin is a matricellular glutamate-containing protein expressed during ontogenesis and in adult connective tissues submitted to mechanical strains including bone and, more specifically, the periosteum, periodontal ligaments, tendons, heart valves, or skin. It is also expressed in neoplastic tissues, cardiovascular and fibrotic diseases, and during wound repair. Its biological functions are extensively investigated in fields such as cardiovascular physiology or oncology. Despite its initial identification in bone, investigations of periostin functions in bone-related physiopathology are less abundant. Recently, several studies have analyzed the potential role of periostin in bone biology and suggest that periostin may be an important regulator of bone formation. The aim of this article is to provide an extensive review on the implications of periostin in bone biology and its potential use in benign and metabolic bone diseases.

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TGF-β1 and FAK Regulate Periostin Expression in PDL Fibroblasts

Cited by 72 publications

References 22 publications

Periostin Mediates TGF-β-Induced Epithelial Mesenchymal Transition in Prostate Cancer Cells

Periostin Mediates TGF-β-Induced Epithelial Mesenchymal Transition in Prostate Cancer Cells

<b>Hertwig’s epithelial root sheath cells contribute to formation of periodontal ligament through epithelial-mesenchymal transition by </b><b>TGF-β </b>

The multiple facets of periostin in bone metabolism

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