EGCG blocks TGFβ1-induced CCN2 by suppressing JNK and p38 in buccal fibroblasts

Chang, Jenny Zwei-Chieng; Yang, Wen-E; Deng, Yi; Chen, Hsin‐Ming; Kuo, Mark Yen‐Ping

doi:10.1007/s00784-012-0713-5

Cited by 27 publications

(41 citation statements)

References 29 publications

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“…If the ECM of the tumour could be modified, then drug penetration into the tumour might be facilitated. Table alludes to effects of various treatment modalities on CAFs.…”

Section: Targeting Of Caf‐related Signalling Pathwaysmentioning

confidence: 99%

“…Curcuminoids (<100 nM) were able to block ECM deposition and TGF‐β/p‐SMAD‐2 signalling pathways in keloid, a fibrotic disease characterised by the abnormal accumulation of ECM in the dermis, with further evidence for anti‐fibrotic effects observed following inhibition of the bleomycin‐induced fibrotic progression in the mouse lung . Another compound with potential anti‐fibrotic activity is the tea polyphenol Epigallocatechin gallate (EGCG), which inhibited TGFβ‐mediated oral submucous fibrosis via suppression of p‐38 mitogen activated protein kinase (p‐38 MAPK) and c‐jun NH2‐terminal kinase (JNK) phosphorylation . Recently, the Src kinase inhibitor Saracatinib (AZD0530) was shown to prevent TGF‐β‐induced Src activation in human lung fibroblasts, preventing transition to a myofibroblast phenotype …”

Section: Targeting Of Caf‐related Signalling Pathwaysmentioning

confidence: 99%

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The role of stromal fibroblasts in lung carcinogenesis: A target for chemoprevention?

et al. 2015

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The tumour microenvironment plays an essential role in the development and spread of cancers. Tumour cells interact with the surrounding extracellular matrix (ECM), embedded within which, are a variety of non‐cancer cells including cells of the vasculature, immune system and fibroblasts. The essential role of fibroblasts in the cultivation and maintenance of an environment in which tumour cells are able to maintain their aggressive phenotypic traits is becoming increasingly well documented. Cancer‐associated fibroblasts are able to secrete a vast array of ECM‐modulating factors, meaning that they have potential for a functional role in every step of the carcinogenic process. In particular, they are likely to have a role in early tumour‐initiating inflammatory events, and so may provide a potential target for chemopreventive intervention. This review summarises the known interactions between lung tumour cells and surrounding reactive fibroblasts, highlighting the need to further investigate cancer‐associated fibroblasts as therapeutic targets in lung cancer chemoprevention strategies.

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“…If the ECM of the tumour could be modified, then drug penetration into the tumour might be facilitated. Table alludes to effects of various treatment modalities on CAFs.…”

Section: Targeting Of Caf‐related Signalling Pathwaysmentioning

confidence: 99%

Section: Targeting Of Caf‐related Signalling Pathwaysmentioning

confidence: 99%

The role of stromal fibroblasts in lung carcinogenesis: A target for chemoprevention?

et al. 2015

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“…76 TGF β is implicated as one of the main triggers for the increased collagen production and decreased matrix degradation pathways in OSF. 52,77 It has been shown that the expression of TGF-β1 was significantly upregulated within the connective tissue of OSF compared to normal mucosa. 62 Treatment of cells with arecanut water extract consisting of polyphenols and alkaloids, has shown that 64% of the differentially regulated genes found in test samples matches with the TGF β induced gene expression profile.…”

Section: Inflammatory Cytokines and Growth Factorsmentioning

confidence: 99%

“…Epigallocatechin-3-gallate (EGCG) in turn can completely block TGF β1 induced CCN2 synthesis by suppressing JNK and p38 in buccal mucosal fibroblasts, which may be useful in controlling OSF. 77 Loss of adipose tissue in OSF was found to be due the ability of TGF β to cause lipodystrophy. Level of TGF β secretion is more during the early course of the disease.…”

mentioning

confidence: 99%

Oral submucous fibrosis: a historical perspective and a review on etiology and pathogenesis

Tilakaratne

Ekanayaka

Warnakulasuriya

2016

Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology

149

126

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“…In an attempt to understand the changes in cytokine levels, gene expression profiling was performed in OSF tissues. The results revealed upregulation of an array of cytokines namely, TGF β 1, TGF β 1p, THBS1, SPP1, TIG1, TGM2 and CTGF and down regulation of BMP7 which is a known negative modulator of fibrosis [24]. TGF β is considered to be a potent stimulator of production and deposition of ECM [25].…”

Section: Growth Factors and Inflammatory Cytokinesmentioning

confidence: 99%

Oral Submucous Fibrosis: Review on Mechanisms of Pathogenesis and Malignant Transformation

Ekanayaka¹,

Tilakaratne²

2013

J Carcinog Mutagen

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Studies focusing on epidemiology, histopathology and molecular biology/pathology on various aspects of oral submucous fibrosis (OSF), especially in the last decade have helped to understand the pathogenesis to a larger extent. In addition research in some aspects of carcinogenesis in the background of fibrosis has also advanced significantly in the recent past allowing us to understand the mechanisms involved in malignant transformation of the most prevalent oral potentially malignant disorder in South Asia. It has been shown that pathogenesis of OSF is directly related to arecoline present in arecanut and most of the alterations in various pathways and molecules leading to accumulation of collagen are mediated as a result of arecoline. Reduction of Matrix metalloproteinases (MMPs) and increased secretion of Tissue inhibitors of matrix metalloproteinases (TIMPs) play the most significant role in collagen accumulation whilst fibrogenic cytokines, mainly TGF-β over expression leads to increased production of collagen. There are various other pathways/molecules contributing to the pathogenesis in varying capacities. Malignant transformation in OSF has also been studied by various groups in the recent past. Role of arecanut as a carcinogen is proven beyond doubt with a large number of animal studies demonstrating its carcinogenicity, mutagenicity and genotoxicity. Studies involved in many molecules implicated in cell cycle regulation, hypoxia, processes leading to DNA double strand breaks, senescence and many other pathways related to carcinogenesis have shown ample evidence for the arecanut induced malignant transformation in OSF. Some of the findings in these studies may be helpful in inventing new treatment strategies for a common disease without an effective treatment up to date. Further, the understanding of mechanisms of malignant transformation may lead to early diagnosis of oral squamous cell carcinoma (OSCC) arising in the background of OSF.

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EGCG blocks TGFβ1-induced CCN2 by suppressing JNK and p38 in buccal fibroblasts

Cited by 27 publications

References 29 publications

The role of stromal fibroblasts in lung carcinogenesis: A target for chemoprevention?

The role of stromal fibroblasts in lung carcinogenesis: A target for chemoprevention?

Oral submucous fibrosis: a historical perspective and a review on etiology and pathogenesis

Oral Submucous Fibrosis: Review on Mechanisms of Pathogenesis and Malignant Transformation

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