MMP-13 is involved in oral cancer cell metastasis

Huang, Shun; Law, Ching Hsuan; Kuo, Ping Hsueh; Hu, Ren; Yang, Congqiao; Chung, Ting; Li, Ji Min; Lin, Li Hsun; Liu, Yi‐Chung; Liao, En Chi; Tsai, Yi Ting; Wei, Yu Shan; Lin, Chi Chen; Chang, Chia-Wei; Chou, Hsiu Chuan; Wang, Wen-Ching; Chang, Ming Che; Wang, Lu Hai; Kung, Hsing Jien; Chan, Hong Lin; Lyu, Ping

doi:10.18632/oncotarget.7942

Cited by 21 publications

(21 citation statements)

References 57 publications

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“…Deraz et al [32] revealed that the overexpression of MMP-10 could promote the invasion and metastasis of head and neck squamous cell carcinoma, and invasion driven by MMP-10 is possibly associated with p38 MAPK inhibition. It has been reported that MMP-13 could promote the invasion, migration, and adhesion abilities of oral cancer cells [33]. The abnormal expression of MMP-7 has been found to be closely related to the biological behaviour of OSCC, and MMP-7 may be Note: the miRNA names in red color are validated using qRT-PCR induced by COX-2 to contribute to the invasion and metastasis of OSCC [34].…”

Section: Discussionmentioning

confidence: 99%

Differential expression of matrix metalloproteinases and miRNAs in the metastasis of oral squamous cell carcinoma

Ren

Yang

et al. 2020

BMC Oral Health

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Background: Our study aimed to reveal the regulatory mechanisms of miRNAs and matrix metalloproteinases (MMPs) in oral squamous cell carcinoma (OSCC). Methods: The mRNA and miRNA expression profiles of six metastatic tumour samples, six nonmetastatic tumour samples, and six normal tissue samples were used for microarray analysis. Moreover, the important genes and miRNAs were validated by published profiles in Oncomine and by qRT-PCR. Results: MMP7, MMP13, and MMP10 were upregulated, and MMP12 and MMP9 were downregulated in metastatic tumours compared with nonmetastatic tumours. MMP7 was regulated by miR-4697-5p and miR-7109-5p. MMP7 and MMP13 were upregulated in OSCC samples compared with normal samples in Oncomine. Moreover, qRT-PCR revealed that the expression of miR-7109-5p and miR-34b was decreased in metastatic tumours compared with nonmetastatic tumours. Conclusions: Our study suggested that miR-7109-5p and miR-34b might play important roles in the metastasis of OSCC by regulating MMP7 and MMP13 expression, respectively.

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Section: Discussionmentioning

confidence: 99%

Differential expression of matrix metalloproteinases and miRNAs in the metastasis of oral squamous cell carcinoma

Ren

Yang

et al. 2020

BMC Oral Health

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“…Despite the general notion that collagenases (MMP1, MMP8 and MMP13) are key players in cancer biology [27][28][29], relatively little is known about collagenases in PDAC. Although MMP-1 is consistently shown to be overexpressed in PDAC patients compared to healthy controls [30][31][32][33][34][35][36], its effects on cancer progression are inconsistent ( Table 1).…”

Section: Collagenases In Pdacmentioning

confidence: 99%

Matrix Metalloproteases in Pancreatic Ductal Adenocarcinoma: Key Drivers of Disease Progression?

Slapak

Duitman

Tekin

et al. 2020

Biology

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Pancreatic cancer is a dismal disorder that is histologically characterized by a dense fibrotic stroma around the tumor cells. As the extracellular matrix comprises the bulk of the stroma, matrix degrading proteases may play an important role in pancreatic cancer. It has been suggested that matrix metalloproteases are key drivers of both tumor growth and metastasis during pancreatic cancer progression. Based upon this notion, changes in matrix metalloprotease expression levels are often considered surrogate markers for pancreatic cancer progression and/or treatment response. Indeed, reduced matrix metalloprotease levels upon treatment (either pharmacological or due to genetic ablation) are considered as proof of the anti-tumorigenic potential of the mediator under study. In the current review, we aim to establish whether matrix metalloproteases indeed drive pancreatic cancer progression and whether decreased matrix metalloprotease levels in experimental settings are therefore indicative of treatment response. After a systematic review of the studies focusing on matrix metalloproteases in pancreatic cancer, we conclude that the available literature is not as convincing as expected and that, although individual matrix metalloproteases may contribute to pancreatic cancer growth and metastasis, this does not support the generalized notion that matrix metalloproteases drive pancreatic ductal adenocarcinoma progression.

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“…The role of MMPs as EMT inducers has been described in kidney, lung, ovary, oral, and mammary epithelium [52][53][54][55][56][57]. Their mechanism of action involves the processing and activation of pro-TGF-β in the ECM, as well as the direct proteolysis of E-cadherin [53,55,57].…”

Section: The Epithelium To Mesenchymal Transitionmentioning

confidence: 99%

Nucleotides and nucleoside signaling in the regulation of the epithelium to mesenchymal transition (EMT)

Martinez-Ramirez

Dı́az-Muñoz

Butanda-Ochoa

et al. 2016

Purinergic Signalling

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The epithelium-mesenchymal transition (EMT) is an important process of cell plasticity, consisting in the loss of epithelial identity and the gain of mesenchymal characteristics through the coordinated activity of a highly regulated informational program. Although it was originally described in the embryonic development, an important body of information supports its role in pathology, mainly in cancerous and fibrotic processes. The purinergic system of inter-cellular communication, mainly based in ATP and adenosine acting throughout their specific receptors, has emerged as a potent regulator of the EMT in several pathological entities. In this context, cellular signaling associated to purines is opening the understanding of a new element in the complex regulatory network of this phenotypical differentiation process. In this review, we have summarized recent information about the role of ATP and adenosine in EMT, as a growing field with high therapeutic potential.Keywords P2 receptors . P1 receptors . Purinergic signaling . Cell migration . EMTThe purinergic system of intercellular communication General aspects The term purine (from: pure urine) was created more than 130 years ago by Emil Fischer after detailed analytical characterization of the uric acid molecule [1]. Purine molecular structure is the result of fusing pyrimidine and imidazole rings, and it exists as four N-H tautomeric forms [2]. Tautomerism of purine bases in DNA is one of the earliest reasons for mutations [3][4][5]. The interconversion of the different adenine or guanine tautomers produced mispairing with pyrimidines (which also show tautomeric forms) that may lead to changes in DNA sequence [6].Purine molecules appeared very early in the history of our planet, in the period known as Borganic evolution^, before the establishment of living systems. It has been postulated that purines could be formed by a eutectic (denoting a mixture of substances in fixed proportions that melts and freezes at a single temperature that is lower than the melting points of any of the separate constituents) concentration of HCN at extremely low temperature over a period of dozens of years [7]. Purine molecules, such as adenine and guanine, are components of the genetic material (DNA and RNA) of all living beings. Purine and pyrimidine tautomeric equilibria in nucleic acids was postulated to be significant in events such as DNA replication and repair as well as in the occurrence of point mutations [8].As nucleosides and nucleotides, purines play other highly strategic roles, acting as energy intermediates, allosteric regulators of key metabolic activities, redox molecules, and chemical messengers for signal transduction events. The two most important purines serving as extracellular ligands for paracrine and autocrine signaling are ATP and its dephosphorylated form, adenosine (ADO). ATP and ADO act as intracellular intermediate metabolites, and their presence in the

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MMP-13 is involved in oral cancer cell metastasis

Cited by 21 publications

References 57 publications

Differential expression of matrix metalloproteinases and miRNAs in the metastasis of oral squamous cell carcinoma

Differential expression of matrix metalloproteinases and miRNAs in the metastasis of oral squamous cell carcinoma

Matrix Metalloproteases in Pancreatic Ductal Adenocarcinoma: Key Drivers of Disease Progression?

Nucleotides and nucleoside signaling in the regulation of the epithelium to mesenchymal transition (EMT)

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