Half-life of synovial cell collagenase mRNA is modulated by phorbol myristate acetate but not by all-trans-retinoic acid or dexamethasone

Brinckerhoff, Constance E.; Plucinska, Izabela M.; Sheldon, Lynn A.; O’Connor, Gerald T.

doi:10.1021/bi00369a006

Cited by 139 publications

(70 citation statements)

References 37 publications

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“…Moreover, in experiments using actinomycin D (1 g/ml) to inhibit mRNA synthesis in H508 cells (see MATERIALS AND METHODS), half-lives of MMP1 and MMP10 mRNA, ϳ24 and 18 h, respectively, were not altered by ACh (data not shown). The half-lives of MMP genes in H508 cells were comparable to those reported by others using different cell lines (3,24,33). These findings indicate that, as observed with MMP7, induction of MMP1 and MMP10 mRNA levels by ACh at 4 -6 h is primarily a consequence of increased transcription, not reduced degradation of mRNA transcripts.…”

Section: Ach-induced Mmp7 Gene Transcription Is Mediated By Transactisupporting

confidence: 87%

Acetylcholine-induced activation of M₃ muscarinic receptors stimulates robust matrix metalloproteinase gene expression in human colon cancer cells

Xie¹,

Cheng²,

Shant³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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ously, we showed that ACh-induced proliferation of human colon cancer cells is mediated by transactivation of epidermal growth factor (EGF) receptors (EGFRs). In the present study, we elucidate the molecular mechanism underlying this action. ACh-induced proliferation of H508 colon cancer cells, which express exclusively M3 muscarinic receptors (M3Rs), was attenuated by anti-EGFR ligand binding domain antibody, a broad-spectrum matrix metalloproteinase (MMP) inhibitor, anti-MMP7 antibody, a diphtheria toxin analog that blocks release of an EGFR ligand [heparin-binding EGF-like growth factor (HBEGF)], and anti-HBEGF antibody. Conditioned media from ACh-treated H508 cells induced proliferation of SNU-C4 colon cancer cells that express EGFR but not M3R. These actions were attenuated by an EGFR inhibitor and by anti-EGFR and anti-HBEGF antibodies. In H508, but not SNU-C4, colon cancer cells, ACh caused a striking dose-and time-dependent increase in levels of MMP7 mRNA and MMP7 protein. Similarly, ACh induced robust MMP1 and MMP10 gene transcription. ACh-induced MMP1, MMP7, and MMP10 gene transcription was attenuated by atropine, anti-EGFR antibody, and chemical inhibitors of EGFR and ERK activation. In contrast, inhibitors of phosphatidylinositol 3-kinase and NF-B activation did not alter MMP gene transcription. Collectively, these findings indicate that MMP7-catalyzed release of HBEGF mediates ACh-induced transactivation of EGFR and consequent proliferation of colon cancer cells. ACh-induced activation of EGFR and downstream ERK signaling also regulates transcriptional activation of MMP7, thereby identifying a novel feed-forward mechanism for neoplastic cell proliferation. epidermal growth factor receptor; gene transcription; heparin-binding epidermal growth factor-like growth factor COLON CANCER, A COMMON and frequently lethal disease, progresses in a multistep process that involves tumor initiation and promotion. Therapeutic strategies directed at interfering with tumor promotion are of particular interest, because this is generally a reversible, long-term process (13). Hence, there is great interest in identifying key colon cancer growth factors and their receptors. Increasing evidence indicates that muscarinic receptors and ligands play key roles in intestinal neoplasia (8,9,14,15,17,27). The muscarinic cholinergic family of G proteincoupled receptors (GPCRs) consists of five muscarinic receptor subtypes designated M 1 R, M 2 R, M 3 R, M 4 R, and M 5 R (for reviews see Refs. 34 and 35). Using RT-PCR with primers specific for muscarinic receptor subtypes, Frucht and colleagues (14, 15) reported that 60% of colon cancer cell lines tested express M 3 R. Follow-up studies revealed that normal colon epithelial cells uniformly express M 3 R, and in 62% of colon cancers, M 3 R expression was increased up to eightfold compared with adjacent normal colon epithelium (37).Work from our laboratory extended these observations by showing that cholinergic ligand-induced proliferation of H508 human colon cancer cells, which exp...

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Section: Ach-induced Mmp7 Gene Transcription Is Mediated By Transactisupporting

confidence: 87%

Acetylcholine-induced activation of M₃ muscarinic receptors stimulates robust matrix metalloproteinase gene expression in human colon cancer cells

Xie¹,

Cheng²,

Shant³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…4). It is conceivable that TGF-␤, in addition to activating the collagenase promoter, may also increase collagenase gene expression by post-transcriptional mechanisms such as stabi- lization of the corresponding mRNA, as described previously for phorbol esters or epidermal growth factor (20,21).…”

Section: Fig 1 Effect Of Tgf-␤ On Collagenase Gene Expression In Dementioning

confidence: 80%

Cell-specific Induction of Distinct Oncogenes of the Jun Family Is Responsible for Differential Regulation of Collagenase Gene Expression by Transforming Growth Factor-β in Fibroblasts and Keratinocytes

Mauviel

Chung

Agarwal

et al. 1996

Journal of Biological Chemistry

148

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Transforming growth factor-␤ (TGF-␤) plays a major role in regulating connective tissue deposition by controlling both extracellular matrix production and degradation. In this study, we show that TGF-␤ transcriptionally represses both basal and tumor necrosis factor-␣-induced collagenase (matrix metalloprotease-1) gene expression in dermal fibroblasts in culture, whereas it activates its expression in epidermal keratinocytes. We demonstrate that this differential effect of TGF-␤ on collagenase gene expression is due to a cell type-specific induction of distinct oncogenes of the Jun family, which participate in the formation of AP-1 complexes with different trans-activating properties. Specifically, our data indicate that the inhibitory effect of TGF-␤ in fibroblasts is likely to be mediated by jun-B, based on the following observations: (a) TGF-␤ induces high levels of jun-B expression and (b) over-expression of jun-B mimics TGF-␤ effect in inhibiting basal collagenase promoter activity and preventing tumor necrosis factor-␣-induced trans-activation of the collagenase promoter. In contrast, TGF-␤ induction of collagenase gene expression in keratinocytes is preceded by transient elevation of c-jun proto-oncogene expression. Over-expression of c-jun leads to trans-activation of the collagenase promoter in both cell types, suggesting that c-jun is a ubiquitous inducer of collagenase gene expression. Transfection of keratinocytes with an antisense c-jun construct together with a collagenase promoter/reporter gene construct inhibits basal and TGF-␤-induced up-regulation of the collagenase promoter activity, implying that c-jun mediates TGF-␤ effect in this cell type. Collectively, our data suggest differential signaling pathways for TGF-␤ in dermal fibroblasts and epidermal keratinocytes, leading to cell type-specific induction of two AP-1 components with opposite transcriptional activities.

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“…This may be due to increased mRNA stability, as suggested for TPA, or EGF [Brinckerhoff et a]., 1986;Delany and Brinckerhoff, 19921. IL-1, TNF-a, and LR stimulation may also result in increased mRNA stability.…”

Section: Of Ap-1 In Transcriptional Regulationmentioning

confidence: 96%

Cytokine regulation of metalloproteinase gene expression

Mauviel

1993

J of Cellular Biochemistry

402

239

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Matrix metalloproteinases belong to a family of zinc-dependent enzymes capable of degrading extracellular matrix and basement membrane components. Their expression is greatly modulated by cytokines and growth factors and involves the gene products of the Fos and Jun families of oncogenes. After extra(peri)cellular activation, their activity can be further controlled by specific tissue inhibitors of metalloproteinases. A correct balance between these regulatory mechanisms is necessary to ensure matrix remodeling in normal physiological processes such as embryonic development, but the overexpression of these enzymes may initiate or contribute to pathological situations such as cartilage degradation in rheumatoid arthritis or to tumor progression and metastasis. Delineation of the mechanisms of metalloproteinase and metalloproteinase inhibitors gene expression, understanding of their mode of interactions, and characterization of their patterns of expression in various tissues in normal and pathological states will lead to new therapeutic strategies to counteract the deleterious effects of matrix metalloproteinases in human disease. Q 1993 WiIey-Liss, Inc.

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Half-life of synovial cell collagenase mRNA is modulated by phorbol myristate acetate but not by all-trans-retinoic acid or dexamethasone

Cited by 139 publications

References 37 publications

Acetylcholine-induced activation of M₃ muscarinic receptors stimulates robust matrix metalloproteinase gene expression in human colon cancer cells

Acetylcholine-induced activation of M₃ muscarinic receptors stimulates robust matrix metalloproteinase gene expression in human colon cancer cells

Cell-specific Induction of Distinct Oncogenes of the Jun Family Is Responsible for Differential Regulation of Collagenase Gene Expression by Transforming Growth Factor-β in Fibroblasts and Keratinocytes

Cytokine regulation of metalloproteinase gene expression

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Half-life of synovial cell collagenase mRNA is modulated by phorbol myristate acetate but not by all-trans-retinoic acid or dexamethasone

Cited by 139 publications

References 37 publications

Acetylcholine-induced activation of M3 muscarinic receptors stimulates robust matrix metalloproteinase gene expression in human colon cancer cells

Acetylcholine-induced activation of M3 muscarinic receptors stimulates robust matrix metalloproteinase gene expression in human colon cancer cells

Cell-specific Induction of Distinct Oncogenes of the Jun Family Is Responsible for Differential Regulation of Collagenase Gene Expression by Transforming Growth Factor-β in Fibroblasts and Keratinocytes

Cytokine regulation of metalloproteinase gene expression

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Acetylcholine-induced activation of M₃ muscarinic receptors stimulates robust matrix metalloproteinase gene expression in human colon cancer cells

Acetylcholine-induced activation of M₃ muscarinic receptors stimulates robust matrix metalloproteinase gene expression in human colon cancer cells