miR-133a suppresses cell proliferation, migration and invasion in human lung cancer by targeting MMP-14

Xu, Meng; Wang, Yu‐Zhou

doi:10.3892/or.2013.2548

Cited by 43 publications

(29 citation statements)

References 33 publications

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“…MT1-MMP accelerated tumor migration and invasion by inducing the epithelial to mesenchymal transition in prostate and squamous cell carcinoma cells [9]. In addition, our previous study indicated that miR-133a suppresses cell proliferation, migration, and invasion in human lung cancer by targeting MMP-14 [10].…”

Section: Introductionmentioning

confidence: 90%

MT1-MMP is not a good prognosticator of cancer survival: evidence from 11 studies

Lin

et al. 2014

Tumor Biol.

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MT1-MMP exhibits diverse expressions in patients with cancer and could be considered as potential prognostic biomarker of cancer. We performed a meta-analysis aiming to provide more sufficient evidence that MT1-MMP expression is associated with poor overall survival in several types of cancers. We systematically searched the studies from databases and carefully identified based on eligibility criteria. The association between MT1-MMP expression and overall survival in cancers was estimated using Review Manager. A total of 11 literatures which included 1,918 cancer patients were combined in the final analysis. Meta-analysis revealed that MT1-MMP overexpression was associated with an unfavorable overall survival and the pooled hazard ratio (HR) and corresponding 95 % confidence interval (CI) was 2.46 (95 % CI 1.75-3.47). From subgroup analyses, we identified that MT1-MMP was an independent prognostic factor for lung cancer and gastric cancer, and HRs (95 % CI) were 3.73 (95 % CI 2.67-5.21) and 2.46 (95 % CI 1.69-3.59), respectively. In conclusion, MT1-MMP is a potential prognostic factor in human cancers.

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Section: Introductionmentioning

confidence: 90%

MT1-MMP is not a good prognosticator of cancer survival: evidence from 11 studies

Lin

et al. 2014

Tumor Biol.

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“…It has been found that miR-9, miR-133a, and miR-24 bind to the 3′-UTR of MMP-14 (MT1-MMP) mRNA and directly block its translation. [24][25][26] On the other hand, downregulation of miR-199a-5p in a murine wound-healing model promoted angiogenesis in acute wounds via Ets-1 derepression and MMP-1 induction, both in vitro and in vivo. 27 As already mentioned, all members of the MMP family are released as an inactive form -proenzyme.…”

Section: Mmps Expression and Activationmentioning

confidence: 99%

Matrix metalloproteinases in the wound microenvironment: therapeutic perspectives

Krejner¹,

Litwiniuk²,

Grzela³

2016

CWCMR

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Matrix metalloproteinases (MMPs) are key effector molecules responsible for extracellular matrix (ECM) turnover. They are involved in tissue remodeling and regeneration. Although the main targets for MMPs are ECM components, they are also able to digest a variety of non-ECM molecules including cytokines, their receptors, or carriers. Therefore, the activity of the MMPs remains under tight control. However, when controlling mechanisms are ineffective, MMPs may become highly dangerous molecules, which have a strong destructive effect on affected tissues. Apart from cancer metastasis, aneurysm formation, or airway remodeling in asthma, MMPs have also been identified as main detrimental factors in delayed healing of chronic wounds. In this short review, we describe main representatives of MMPs family, their role in pathophysiology of chronic wounds, as well as current and possible therapeutic strategies for modulation of MMPs' activity, which may be useful in management of chronic wounds.

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“…We then examined the effect of PML on the expression of several genes important for cancer metastasis, including MMP2, MMP9, ITGB1 and MMP14. [36][37][38][39] We found that the mRNA expression of MMP2, but not of the other 3 genes, was significantly upregulated in response to PML knockdown ( Fig. 2A and Fig.…”

Section: Pml Suppressed Negfr-induced Mmp2 Expressionmentioning

confidence: 99%

PML represses lung cancer metastasis by suppressing the nuclear EGFR-mediated transcriptional activation ofMMP2

et al. 2014

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Promyelocytic leukemia protein (PML) is emerging as an important tumor suppressor. Its expression is lost during the progression of several types of cancer, including lung cancer. The EGF receptor (EGFR), a membrane-bound receptor tyrosine kinase, transduces intracellular signals responsible for cell proliferation, differentiation and migration. EGFR activity is frequently abnormally upregulated in lung adenocarcinoma (LAC) and thus is considered to be a driving oncogene for LAC. EGFR translocates into the nucleus and transcriptionally activates genes, such as CCND1, that promote cell growth. Recently, we demonstrated that PML interacted with nuclear EGFR (nEGFR) and suppressed the nEGFR-mediated transcriptional activation of CCND1 in lung cancer cells, thereby restraining cell growth. When we further investigated the interplay between PML and EGFR in lung cancer metastasis, we found that the matrix metalloprotease-2 gene (MMP2) was a novel nEGFR target gene and was repressed by PML. We provide evidence that nEGFR bound to the AT-rich sequence (ATRS) in the MMP2 promoter and enhanced its transcriptional activity. In addition, we demonstrated that PML repressed nEGFR-induced MMP2 transcription and reduced cell invasion. PML was recruited by nEGFR to the MMP2 promoter where it reduced histone acetylation, leading to the transcriptional repression of MMP2. Finally, we demonstrated that PML upregulation by interferon-b (IFNb) in lung cancer cells decreased MMP2 expression and cell invasion. Together, our results suggested that IFNb induced PML to inhibit lung cancer metastasis by repressing the nEGFR-mediated transcriptional activation of MMP2.

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miR-133a suppresses cell proliferation, migration and invasion in human lung cancer by targeting MMP-14

Cited by 43 publications

References 33 publications

MT1-MMP is not a good prognosticator of cancer survival: evidence from 11 studies

MT1-MMP is not a good prognosticator of cancer survival: evidence from 11 studies

Matrix metalloproteinases in the wound microenvironment: therapeutic perspectives

PML represses lung cancer metastasis by suppressing the nuclear EGFR-mediated transcriptional activation ofMMP2

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