Jun N-Terminal Kinase 1 Mediates Transcriptional Induction of Matrix Metal loproteinase 9 Expression

Crowe, David L.; Tsang, Kenneth J.; Shemirani, Babak

doi:10.1038/sj.neo.7900135

Cited by 46 publications

(31 citation statements)

References 11 publications

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“…Numerous studies have demonstrated that JNK1/2 and ERK1/2 transcriptionally regulate the expression of MMP-2 and MMP-9, which results in regulation of cell migration and invasion (25)(26)(27). In human bladder cancer cells, upregulation of the MAPK pathways may result in migration and regulation of the expression levels of MMPs (28).…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of resveratrol on the adhesion, migration and invasion of human bladder cancer cells

Bai

Yang

Zhang

et al. 2016

Molecular Medicine Reports

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Abstract.Resveratrol is a polyphenolic compound, which has been revealed to induce apoptosis in numerous human cancer cells; however, the effects of resveratrol on the migration and invasion of human bladder cancer cells have not been reported. The present study aimed to evaluate the anti-metastatic potential of resveratrol against bladder cancer and its mechanism of action. The results indicated that resveratrol inhibits the adhesion, migration and invasion of bladder cancer cells in a dose-dependent manner. Resveratrol was shown to significantly inhibit the expression and secretion of matrix metalloproteinase (MMP)-2 and MMP-9 in bladder cancer cells. Furthermore, resveratrol suppressed the phosphorylation of c-Jun N-terminal kinase and extracellular signal-regulated protein kinase. In conclusion, the present study is the first, to the best of our knowledge, to demonstrate that resveratrol may be considered a novel anticancer agent for the treatment of bladder cancer via the inhibition of migration and invasion. IntroductionBladder cancer is the fourth most common type of cancer, and was the cause of >11,510 cases of cancer-associated mortality among men in the USA in 2014 (1). The majority of bladder cancer cases are noninvasive, low-grade transitional cell carcinoma (TCC); however, ≤30% of all diagnosed tumors are classified as invasive TCC, which is associated with high mortality (2). Notably, among all of the various types of cancer, bladder cancer exhibits a significantly high incidence of recurrence post-treatment, and therefore is recognized as the most expensive cancer to treat. Due to the high prevalence and frequent tumor recurrence associated with bladder cancer, the exploration of preventative strategies is required.Previous epidemiological and scientific studies have indicated that plant-derived phytochemicals may be beneficial in the prevention and treatment of cancer (3-5). Resveratrol is a polyphenolic compound, which is present in grapes (red wine), knotweed, peanuts, mulberries and other plants. Numerous studies have suggested that resveratrol may prevent the progression of various pathologies, including vascular diseases, ischemic injuries, cancer and neurodegenerative disorders (6-8). Furthermore, it has previously been confirmed that resveratrol exerts antiproliferative and/or apoptotic effects on leukemia, prostate, breast and colon cancers cells in vitro (9-12). Previous studies regarding the anticancer effects of resveratrol have focused on its anti-invasive and anti-metastatic activities (13-15). However, to the best of our knowledge, there is currently no evidence as to whether resveratrol may inhibit the migration and invasion of human bladder cancer cells.Metastasis is one of the hallmarks of advanced cancer progression, and cancer cell migration and invasion are crucial events in bladder cancer metastasis. Matrix metalloproteinases (MMPs), including MMP-2 and MMP-9, degrade the basement membrane and extracellular matrix (ECM), and are therefore considered crucial proteolytic protei...

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Section: Discussionmentioning

confidence: 99%

Inhibitory effects of resveratrol on the adhesion, migration and invasion of human bladder cancer cells

Bai

Yang

Zhang

et al. 2016

Molecular Medicine Reports

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“…Several signaling pathways activated downstream from the IGF-IR are also implicated in MMP upregulation. MMP-9 is upregulated by the mitogen-activated protein kinases (MAPKs) and the jun amino-terminal kinases (JNKs) in vascular smooth muscle cells (Cho et al, 2000), human epidermal keratinocytes (Zeigler et al, 1999;McCawley et al, 1999), and in numerous tumor types (Lakka et al, 2000;Gum et al, 1997;Crowe et al, 2001). In v-src transformed cells, which are invasive, MMP-2 is upregulated through constitutive, sustained activation of the MAPK kinase MEK1 (Kurata et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

N-Myc and Bcl-2 coexpression induces MMP-2 secretion and activation in human neuroblastoma cells

Noujaim

Golen

et al. 2002

Oncogene

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“…Phosphorylation of a number of ets family members has been shown to increase CBP/p300 recruitment (10,16,20,27,30). We previously demonstrated that phosphorylation of the AP-1 protein c-jun is a potent activator of MMP-9 expression, suggesting a novel mechanism by which this modification may recruit coactivator proteins (8). These results suggest that phosphorylation of transcription factors and coactivators may provide a rapid means of regulating histone acetylation, chromatin unwinding, and induction of gene transcription.…”

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confidence: 86%

Extracellular Signals Regulate Rapid Coactivator Recruitment at AP-1 Sites by Altered Phosphorylation of both CREB Binding Protein and c-jun

Tsai

Salib

et al. 2008

Molecular and Cellular Biology

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Retinoic acid (RA) inhibits matrix metalloproteinase 9 (MMP-9) expression due to AP-1 inhibition resulting from retinoic acid receptors (RARs) competing for limiting amounts of coactivator proteins. However, given the rapid kinetics of MMP-9 transcription, it seems unlikely that these interactions can be explained passively. Our previous studies indicated that coactivator and transcription factor phosphorylation may allow for rapid regulation of MMP-9 expression. In the present study we tested this hypothesis directly. CREB binding protein (CBP) and p300/CBP-associated factor (PCAF) were displaced from transcription factor binding sites on the MMP-9 promoter within minutes of RA treatment. The RAR interaction domains of CBP and PCAF were not required for this displacement. RA and epidermal growth factor had opposing effects on phosphorylation of CBP by extracellular signal-regulated kinase 1 that correlated with altered CBP occupancy of AP-1 sites and differential MMP-9 promoter activation. We identified a novel phosphorylation site in the CBP carboxyl terminus that mediated association with AP-1 sites in the MMP-9 promoter. Inhibition of c-jun phosphorylation displaced PCAF from AP-1 sites and reduced promoter activity. Phosphorylation deficient c-jun was less able to recruit PCAF to AP-1 sites. We also demonstrated novel interactions between coactivators and AP-1 proteins. We propose that extracellular signal-mediated coactivator exchange at AP-1 sites is mediated via protein kinase pathways.

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Jun N-Terminal Kinase 1 Mediates Transcriptional Induction of Matrix Metal loproteinase 9 Expression

Cited by 46 publications

References 11 publications

Inhibitory effects of resveratrol on the adhesion, migration and invasion of human bladder cancer cells

Inhibitory effects of resveratrol on the adhesion, migration and invasion of human bladder cancer cells

N-Myc and Bcl-2 coexpression induces MMP-2 secretion and activation in human neuroblastoma cells

Extracellular Signals Regulate Rapid Coactivator Recruitment at AP-1 Sites by Altered Phosphorylation of both CREB Binding Protein and c-jun

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