Transforming growth factor-β1 induces epithelial-mesenchymal transition and increased expression of matrix metalloproteinase-16 via miR-200b downregulation in bladder cancer cells

Chen, Min Feng; Feng, Zhaoyong; Qi, Lin; Zu, Xiong; Wang, Jun; Liu, Long Fei; Li, Yuan

doi:10.3892/mmr.2014.2366

Cited by 25 publications

(16 citation statements)

References 24 publications

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“…In fact, in a study focused on melanoma patients, a copy‐number gain or overexpression of MMP‐16 has been determined as a putative indicator of adverse melanoma prognosis, associated with poor clinical outcome, collagen bundle assembly around tumor cell nests, and lymphatic invasion (Tatti et al, ). Other studies have shown that tumor growth factor beta 1 can increase the levels of MMP‐16, eliciting a potential connection with the invasion and metastasis in bladder cancer (Chen et al, ). Some studies investigating the effects of inhibition of the metalloproteinase have reported promising data.…”

Section: Matrix Metalloproteinase‐16mentioning

confidence: 97%

Intricate Functions of Matrix Metalloproteinases in Physiological and Pathological Conditions

Mittal

Patel

Debs

et al. 2016

Journal Cellular Physiology

147

115

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Matrix metalloproteinases (MMPs) are a diverse group of proteolytic enzymes and play an important role in the degradation and remodeling of the extracellular matrix (ECM). In normal physiological conditions, MMPs are usually minimally expressed. Despite their low expression, MMPs have been implicated in many cellular processes ranging from embryological development to apoptosis. The activity of MMPs is controlled at three different stages: (1) transcription; (2) zymogen activation; and (3) inhibition of active forms by tissue inhibitor metalloproteinases (TIMPs). They can collectively degrade any component of ECM and basement membrane, and their excessive activity has been linked to numerous pathologies mainly including, but not limited to, tumor invasion and metastasis. The lack of information about several MMPs and the steady stream of new discoveries suggest that there is much more to be studied in this field. In particular, there is a need for controlling their expression in disease states. Various studies over the past 30 years have found that each MMP has a specific mode of activation, action, and inhibition. Drugs specifically targeting individual MMPs could revolutionize the treatment of a great number of health conditions and tremendously reduce their burden. In this review article, we have summarized the recent advances in understanding the role of MMPs in physiological and pathological conditions. J. Cell. Physiol. 231: 2599-2621, 2016. © 2016 Wiley Periodicals, Inc.

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Section: Matrix Metalloproteinase‐16mentioning

confidence: 97%

Intricate Functions of Matrix Metalloproteinases in Physiological and Pathological Conditions

Mittal

Patel

Debs

et al. 2016

Journal Cellular Physiology

147

115

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“…These findings suggest and an association between TGF-β1, MMP-16 and epithelial-mesenchymal transition, in the setting of tumor invasion and metastasis in bladder cancer. 152 …”

Section: Special Attributes Of Specific Mmpsmentioning

confidence: 99%

Biochemical and Biological Attributes of Matrix Metalloproteinases

Cui

Khalil

2017

Progress in Molecular Biology and Translational Science

1,005

891

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Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that are involved in the degradation of various proteins in the extracellular matrix (ECM). Typically, MMPs have a propeptide sequence, a catalytic metalloproteinase domain with catalytic zinc, a hinge region or linker peptide, and a hemopexin domain. MMPs are commonly classified on the basis of their substrates and the organization of their structural domains into collagenases, gelatinases, stromelysins, matrilysins, membrane-type (MT)-MMPs, and other MMPs. MMPs are secreted by many cells including fibroblasts, vascular smooth muscle (VSM) and leukocytes. MMPs are regulated at the level of mRNA expression and by activation of their latent zymogen form. MMPs are often secreted as inactive proMMP form which is cleaved to the active form by various proteinases including other MMPs. MMPs cause degradation of ECM proteins such as collagen and elastin, but could influence endothelial cell function as well as VSM cell migration, proliferation, Ca2+ signaling and contraction. MMPs play a role in tissue remodeling during various physiological processes such as angiogenesis, embryogenesis, morphogenesis and wound repair, as well as in pathological conditions such as myocardial infarction, fibrotic disorders, osteoarthritis, and cancer. Increases in specific MMPs could play a role in arterial remodeling, aneurysm formation, venous dilation and lower extremity venous disorders. MMPs also play a major role in leukocyte infiltration and tissue inflammation. MMPs have been detected in cancer, and elevated MMP levels have been associated with tumor progression and invasiveness. MMPs can be regulated by endogenous tissue inhibitors of metalloproteinases (TIMPs), and the MMP/TIMP ratio often determines the extent of ECM protein degradation and tissue remodeling. MMPs have been proposed as biomarkers for numerous pathological conditions and are being examined as potential therapeutic targets in various cardiovascular and musculoskeletal disorders as well as cancer.

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“…According to another study, miR-200b targets and inhibits the expression of MMP16. TGF-β1-mediated repression miR-200b leads to activation of MMP16 expression and stimulation of the migration of bladder cancer cells [297]. TGF-β1-induced expression of oncogenic miR-221 triggers EMT and stimulates the migration and invasion of bladder cancer cells [298].…”

Section: Bladder Cancermentioning

confidence: 99%

TGF-β and microRNA Interplay in Genitourinary Cancers

Bogusławska¹,

Kryst

Poletajew

et al. 2019

Cells

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Genitourinary cancers (GCs) include a large group of different types of tumors localizing to the kidney, bladder, prostate, testis, and penis. Despite highly divergent molecular patterns, most GCs share commonly disturbed signaling pathways that involve the activity of TGF-β (transforming growth factor beta). TGF-β is a pleiotropic cytokine that regulates key cancer-related molecular and cellular processes, including proliferation, migration, invasion, apoptosis, and chemoresistance. The understanding of the mechanisms of TGF-β actions in cancer is hindered by the “TGF-β paradox” in which early stages of cancerogenic process are suppressed by TGF-β while advanced stages are stimulated by its activity. A growing body of evidence suggests that these paradoxical TGF-β actions could result from the interplay with microRNAs: Short, non-coding RNAs that regulate gene expression by binding to target transcripts and inducing mRNA degradation or inhibition of translation. Here, we discuss the current knowledge of TGF-β signaling in GCs. Importantly, TGF-β signaling and microRNA-mediated regulation of gene expression often act in complicated feedback circuits that involve other crucial regulators of cancer progression (e.g., androgen receptor). Furthermore, recently published in vitro and in vivo studies clearly indicate that the interplay between microRNAs and the TGF-β signaling pathway offers new potential treatment options for GC patients.

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Transforming growth factor-β1 induces epithelial-mesenchymal transition and increased expression of matrix metalloproteinase-16 via miR-200b downregulation in bladder cancer cells

Cited by 25 publications

References 24 publications

Intricate Functions of Matrix Metalloproteinases in Physiological and Pathological Conditions

Intricate Functions of Matrix Metalloproteinases in Physiological and Pathological Conditions

Biochemical and Biological Attributes of Matrix Metalloproteinases

TGF-β and microRNA Interplay in Genitourinary Cancers

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