2017
DOI: 10.1038/s41598-017-08581-y
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Novel STAT binding elements mediate IL-6 regulation of MMP-1 and MMP-3

Abstract: Dynamic remodelling of the extracellular matrix (ECM) is a key feature of cancer progression. Enzymes that modify the ECM, such as matrix metalloproteinases (MMPs), have long been recognised as important targets of anticancer therapy. Inflammatory cytokines are known to play a key role in regulating protease expression in cancer. Here we describe the identification of gamma-activated site (GAS)-like, signal transducer and activator of transcription (STAT) binding elements (SBEs) within the proximal promoters … Show more

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Cited by 24 publications
(20 citation statements)
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“…In contrast, IL6/sIL6R effect on these genes seems to be more specific. For instance, MMP1 and MMP3 genes bear STAT binding sites [ 43 ] that would make them susceptible of IL6-induction by promoter-bound STAT3 or STAT1, in contrast to other MMPs gene promoters that do not have STAT motifs [ 44 ]. Although differences in the cell sources used in both studies may account for part of the discrepancies between Araki’s results [ 41 ] and ours, the fact that MMP3 is not expressed at any dose tested, even under active transcriptional conditions such as those imposed by TNFα, suggests that IL6 does not induce the recruitment of transcription factors to the MMP3 promoter, further supporting that de novo transcription has a major role in the response mediated by IL6/sIL6R signaling.…”
Section: Discussionmentioning
confidence: 99%
“…In contrast, IL6/sIL6R effect on these genes seems to be more specific. For instance, MMP1 and MMP3 genes bear STAT binding sites [ 43 ] that would make them susceptible of IL6-induction by promoter-bound STAT3 or STAT1, in contrast to other MMPs gene promoters that do not have STAT motifs [ 44 ]. Although differences in the cell sources used in both studies may account for part of the discrepancies between Araki’s results [ 41 ] and ours, the fact that MMP3 is not expressed at any dose tested, even under active transcriptional conditions such as those imposed by TNFα, suggests that IL6 does not induce the recruitment of transcription factors to the MMP3 promoter, further supporting that de novo transcription has a major role in the response mediated by IL6/sIL6R signaling.…”
Section: Discussionmentioning
confidence: 99%
“…For most of the MMPs, TNFα induces activation via several transcription factors, including NF-kB and activator protein 1 (AP-1) [43]. In contrast, IL6/sIL6R effect on these genes seems to be more speci c. For instance, mmp1 and mmp3 genes bear STAT binding sites [44] that would make them susceptible of IL6induction by promoter-bound STAT3 or STAT1, in contrast to other MMPs gene promoters that do not have STAT motifs [45]. Although differences in the cell sources used in both studies may account for part of the discrepancies between Araki´s results [42] and ours, the fact that mmp3 is not expressed at any dose tested, even under active transcriptional conditions such as those imposed by TNFα, suggests that IL6 does not induce the recruitment of transcription factors to the mmp3 promoter, further supporting that de novo transcription has a major role in the response mediated by IL6/sIL6R signaling.…”
Section: Discussionmentioning
confidence: 99%
“…For most of the MMPs, TNFα induces activation via several transcription factors, including NF-kB and activator protein 1 (AP-1) [43]. In contrast, IL6/sIL6R effect on these genes seems to be more speci c. For instance, mmp1 and mmp3 genes bear STAT binding sites [44] that would make them susceptible of IL6induction by promoter-bound STAT3 or STAT1, in contrast to other MMPs gene promoters that do not have STAT motifs [45]. Although differences in the cell sources used in both studies may account for part of the discrepancies between Araki´s results [42] and ours, the fact that mmp3 is not expressed at any dose tested, even under active transcriptional conditions such as those imposed by TNFα, suggests that IL6 does not induce the recruitment of transcription factors to the mmp3 promoter, further supporting that de novo transcription has a major role in the response mediated by IL6/sIL6R signaling.…”
Section: Discussionmentioning
confidence: 99%