Epidermal Growth Factor Induces CD44 Gene Expression through a Novel Regulatory Element in Mouse Fibroblasts

Zhang, Ming; Wang, Ming Hui; Singh, Raj K.; Wells, Alan; Siegal, Gene P.

doi:10.1074/jbc.272.22.14139

Cited by 44 publications

(31 citation statements)

References 34 publications

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“…This sequence spanned part of the promoter sequence and the flanking 100 bp of the 5'-sequence of the CD44 gene (71000/+100), linked to pGL3-B which contains the luciferase gene to generate pCD44(71000/+100)-luc. We identified a 22-bp consensus regulatory element to EGF (ERE) within this sequence, between -604 to -583, supporting previous findings (Shtivelman and Bishop, 1991;Zhang et al, 1997). Then, twobase-targeted mutations of this sequence at ERE site (7604 and -583) were obtained.…”

Section: Discussionsupporting

confidence: 83%

“…The PCR fragment was subcloned into pSP72 (Promega) and automatically sequenced as described. The nested PCR showed that the promoter sequence is similar to that published previously (Shtivelman and Bishop, 1991) and includes the ERE motif between -604 and -583, as described (Shtivelman and Bishop, 1991;Zhang et al, 1997). The resultant 1100 bp fragment was subcloned upstream of the luciferase reporter plasmid pGL3-Basic which contains the luciferase gene to generate pCD44(71000/+100)-luc.…”

Section: Fluorescence-activated Cell Sorter (Facs) Analysismentioning

confidence: 79%

“…Synthetic oligonucleotides of the putative ERE sequence (Zhang et al, 1997) and sequences from the mutated ERE oligonucleotides (5'-CCCTCTCCCCAGCTCCCCTCCC-3') OR (5'-CCCTCTATCCAGCTCCTATCCC-3') were annealed and 5'-endlabelled with g-32 P-ATP by T4 kinase (BioLab New England, Beverly, MA, USA). Each probe (2610 4 c.p.m.)…”

Section: Gel Shift Mobility Assaymentioning

confidence: 99%

“…This epidermal growth factor (EGF) regulatory element (ERE) sequence of CD44 (Shtivelman and Bishop, 1991), unlike other cis-acting elements that contain the Sp1 site, comprises a specifically oriented 22-bp sequence, necessary to enable EGF-induced CD44 gene transcription through a specific interaction between the ERE motif and an unknown transcription factor. Point mutations within this sequence alter CD44 transcription (Zhang et al, 1997).…”

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confidence: 99%

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Butyrate down-regulates CD44 transcription and liver colonisation in a highly metastatic human colon carcinoma cell line

et al. 2002

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Over-expression of the adhesion molecule CD44 and its splice variants, especially CD44v6, is associated with poor prognosis and metastasis. We aimed at regulating the expression of CD44 in the highly metastatic human colon cancer cell line HM7 and thereby affecting its metastatic ability. HM7 cells show constitutive expression of CD44 standard and variants isoforms, which were significantly down-regulated by treatment with butyrate. Butyrate significantly inhibited transcription of the CD44 gene and abolished epidermal growth factor-mediated up-regulation of the reporter gene luciferase subcloned upstream to the CD44 promoter ( -1.1 kb) and transfected to HM7 cells. Nuclear proteins from butyrate-treated cells bound to an epidermal growth factor receptor element motif present in the CD44 promoter. Epidermal growth factor receptor elementsite directed mutations eliminated the inducibility of the luciferase reporter gene and did not allowed binding of nuclear proteins harvested from butyrate-treated cells. Butyrate induced CD44 gene repression by specifically interacting with an epidermal growth factor receptor element nuclear transcriptional factor. This interaction affects CD44 transcriptional activity vis-à-vis in vivo metastatic ability of HM7 cells. These results provide additional insight into the anticarcinogenic properties of butyrate.

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Section: Discussionsupporting

confidence: 83%

Section: Fluorescence-activated Cell Sorter (Facs) Analysismentioning

confidence: 79%

Section: Gel Shift Mobility Assaymentioning

confidence: 99%

mentioning

confidence: 99%

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Butyrate down-regulates CD44 transcription and liver colonisation in a highly metastatic human colon carcinoma cell line

et al. 2002

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“…145 The discovery of an EGF-responsive element in the CD44 promoter provides evidence for the presence of dysregulated EGF-mediated signaling as a contributor to this process. 171 Further, CD44 upregulation has been linked to enhanced neuregulin-mediated signaling, 140 indicating a potential for the role of a positive feedback mechanism.…”

Section: Progression Pathways-development Of Malignancymentioning

confidence: 99%

Experimental therapeutic approaches to peripheral nerve tumors

Riley¹,

Spiotta

Boulis³

2007

FOC

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✓Discovery that the Schwann cell is the primary cell type responsible for both the neurofibroma as well as the schwannoma has proven to represent a crucial milestone in understanding the pathogenesis of peripheral nerve tumor development. This information and related findings have served as a nidus for research aimed at more fully characterizing this family of conditions. Recent discoveries in the laboratory have clarified an understanding of the molecular mechanisms underlying the pathogenesis of benign peripheral nerve tumors. Similarly, the mechanisms whereby idiopathic and syndromic (NF1- and NF2-associated) nerve sheath tumors progress to malignancy are being elucidated. This detailed understanding of the molecular pathogenesis of peripheral nerve tumors provides the information necessary to create a new generation of therapies tailored specifically to the prevention, cessation, or reversal of pathological conditions at the fundamental level of dysfunction. The authors review the data that have helped to elucidate the molecular pathogenesis of this category of conditions, explore the current progress toward exploitation of these findings, and discuss potential therapeutic avenues for future research.

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Decreased expression of cd44 in metastatic prostate cancer

et al. 1999

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Decreased expression of CD44 is an independent prognostic marker for surgically treated prostate cancer. To investigate immunohistochemically defined CD44 expression in primary and metastatic prostate cancer, 2 groups of patients undergoing radical prostatectomy for clinically localized prostate cancer were studied. (1) pN1 group: 23 patients, finally staged pN1, of whom the radical prostatectomy specimen and the lymph nodes were investigated to establish a correlation between CD44 expression in the concurrently resected primaries and metastases; (2) pN0 group: 23 patients with pN0 disease matched for pT stage and Gleason sum score with the pN1 patients. Progression rates based on serum prostate‐specific antigen (PSA) levels could be determined in 42 of these 46 patients. In addition, 28 distant metastases were studied. A CD44 score of < 10% was found in 22 of the 23 lymph node metastases (96%) and in 20 of the corresponding radical prostatectomies. In the pN0 group this was observed in only 6 out of 23 specimens. In most of the distant metastases CD44 scores were < 10%. Patients with pN0 disease and > 10% CD44‐positive tumor cells had a significantly better prognosis than the other patients who were not significantly different from each other. CD44 expression is thus strongly reduced in prostate cancer metastases as well as in the corresponding primary tumors. This reduction may be used to predict the N stage clinically, provided that CD44 scores can be determined reliably on preoperative biopsy specimens. Int. J. Cancer (Pred. Oncol.) 84:478–483, 1999. © 1999 Wiley‐Liss, Inc.

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Epidermal Growth Factor Induces CD44 Gene Expression through a Novel Regulatory Element in Mouse Fibroblasts

Cited by 44 publications

References 34 publications

Butyrate down-regulates CD44 transcription and liver colonisation in a highly metastatic human colon carcinoma cell line

Butyrate down-regulates CD44 transcription and liver colonisation in a highly metastatic human colon carcinoma cell line

Experimental therapeutic approaches to peripheral nerve tumors

Decreased expression of cd44 in metastatic prostate cancer

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