Transcriptional inactivation of c-myc and the transferrin receptor in dibutyryl cyclic AMP-treated HL-60 cells.

Trepel, Jane B.; Colamonici, O R; Kelly, Kathleen; Schwab, G; Watt, R A; Sausville, E A; Jaffe, E S; Neckers, Leonard Μ.

doi:10.1128/mcb.7.7.2644

Cited by 44 publications

(23 citation statements)

References 28 publications

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“…The p38 pathway also plays an essential role in regulating many cellular processes including inflammation, cell differentiation, cell cycle, cell growth and death [12] . Regarding the effect of cAMP on the cell cycle progression, several reports demonstrated that cAMP could induce G1 synchronization, growth arrest, and terminal differentiation in certain cells [13,14] . For example, Lee et al [15] , showed that cAMP could induce G1 arrest and apoptosis in hepatoma cells.…”

Section: Introductionmentioning

confidence: 99%

Involvement of fatty acid-CoA ligase 4 in hepatocellular carcinoma growth: Roles of cyclic AMP and p38 mitogen-activated protein kinase

Liang

Chu³

et al. 2005

WJG

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AIM: Fatty acid-CoA ligase 4 (FACL4) is an arachidonatepreferring enzyme which has been shown to be up-regulated in human colon cancer tissues and implicated in the colon tumorigenesis. The purpose of this study was to investigate the role of FACL4 in the human hepatocellular carcinoma (HCC) tumorigenesis and the specific signal pathways involved in this process. METHODS:We investigated the expression and regulation of FACL4 in HCC, adjacent non-tumorous liver tissues, and cell lines. RESULTS:In HCC patients, we demonstrated that FACL4 gene expression was markedly elevated in the cancerous tissues than in the adjacent non-cancerous liver tissues. In addition, several human hepatoma cell lines, including Hep3B and HepG2, expressed high levels of FACL4. Stable overex-pression of FACL4 knockdown plasmids (small interfering RNA, siRNA) to Hep3B cells significantly decreased FACL4 expression and subsequently limited the cell proliferation. Treatment of Hep3B cells with 8-bromo-cAMP and SB203508 (p38 MAPK inhibitor) significantly suppressed the FACL4 expression.CONCLUSION: FACL4 is involved in the HCC tumorigenesis and both cAMP and p38 MAPK pathways are associated with the regulation of FACL4 in HCC.

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Section: Introductionmentioning

confidence: 99%

Involvement of fatty acid-CoA ligase 4 in hepatocellular carcinoma growth: Roles of cyclic AMP and p38 mitogen-activated protein kinase

Liang

Chu³

et al. 2005

WJG

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“…We also achieved growth arrest conditions by inducing the differentiation of HL60 cells. Exposure to Bu2AMP or TPA has been shown to induce terminal monocytic differentiation of this promyelocytic cell line (22 with Bu2AMP induced morphologic chat of differentiation, cessation of cell grow decrease in DNA synthesis but induced n or A45 RNA (Fig. 4).…”

mentioning

confidence: 99%

Mammalian genes coordinately regulated by growth arrest signals and DNA-damaging agents.

Fornace¹,

Nebert²,

Hollander³

et al. 1989

Mol. Cell. Biol.

670

433

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More than 20 different cDNA clones encoding DNA-damage-inducible transcripts in rodent cells have recently been isolated by hybridization subtraction (A. J. Fornace, Jr., I. Alamo, Jr., and M. C. Hollander, Proc. Natl. Acad. Sci. USA 85:8800-8804, 1988). In most cells, one effect of DNA damage is the transient inhibition of DNA synthesis and cell growth. We now show that five of our clones encode transcripts that are increased by other growth cessation signals: growth arrest by serum reduction, medium depletion, contact inhibition, or a 24-h exposure to hydroxyurea. The genes coding for these transcripts have been designated gadd (growth arrest and DNA damage inducible). Two of the gadd cDNA clones were found to hybridize at high stringency to transcripts from human cells that were induced after growth cessation signals or treatment with DNA-damaging agents, which indicates that these responses have been conserved during mammalian evolution. In contrast to results with growth-arrested cells that still had the capacity to grow after removal of the growth arrest conditions, no induction occurred in HL60 cells when growth arrest was produced by terminal differentiation, indicating that only certain kinds of growth cessation signals induce these genes. All of our experiments suggest that the gadd genes are coordinately regulated: the kinetics of induction for all five transcripts were similar; in addition, overexpression of gadd genes was found in homozygous deletion c14CoS/c14CoS mice that are missing a small portion of chromosome 7, suggesting that a trans-acting factor encoded by a gene in this deleted portion is a negative effector of the gadd genes. The gadd genes may represent part of a novel regulatory pathway involved in the negative control of mammalian cell growth.

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“…A major RNA cap site was mapped by primer extension downstream of the GC-rich stretch with several consensus sites for the transcription factor SPl, including SPl sites, which partly overlapped the consensus sites for the GC factor, reported to repress transcriptional activation of the EGF receptor gene [22]. Proximal to that cluster, an AP2 site, previously described as responsive to CAMP and TPA [23,24], was located. The promoter proximal part conferred maximal activity in a transient transfection assay.…”

Section: Discussionmentioning

confidence: 99%

“…None of these cell lines express detectable amounts of RNA St. The transfected cells were then stimulated with TPA, 24], or dexamethasone [25]. All three compounds elicited minor or no detectable effects compared to the untreated control (data not shown).…”

Section: Deletional Analysis Of the Plc?$ Promotermentioning

confidence: 99%

Cloning and functional analysis of the hematopoietic cell‐specific phospholipase Cγ² promoter

et al. 1996

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Phospholipase C$ (PLC-& is a phospholipid-converting enzyme which, upon receptor stimulation, is activated within membrane-bound signalllng complexes. In contrast to the highly ubiquitous PLCy', PLCJ is expressed predominantly in B-lymphocytes. Associated with antigen-coupling receptors it is activated by tyrosine phosphorylation after the triggering of Bcell surface immunoglobulin. We have cloned and sequenced the human PLCJ promoter. Primer extension analysis reveals the existence of a major transcriptional start site. The TATA-less promoter contains G+C-rich stretches with a cluster of contiguous SPl consensus sites, an NFl, and an AP2 site between bp -220 to -70. A construct containing the region from -189 to +78 confers full promoter activity, as shown by fusion to a luciferase reporter gene construct. The distal part of the promoter between bp -662 to -293 containing an SRE, EBF and CACCC box contributed negatively to promoter activity in the B-cell line Raji but not in three adherent cell lines. In Raji cells, PLCJ mRNA is expressed at low levels with a half life greater than 4 h. After treatment with serum, TPA, retinoic acid, or with 5azacytidine increased levels of PLC? mRNA were induced in B-cells.

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Transcriptional inactivation of c-myc and the transferrin receptor in dibutyryl cyclic AMP-treated HL-60 cells.

Cited by 44 publications

References 28 publications

Involvement of fatty acid-CoA ligase 4 in hepatocellular carcinoma growth: Roles of cyclic AMP and p38 mitogen-activated protein kinase

Involvement of fatty acid-CoA ligase 4 in hepatocellular carcinoma growth: Roles of cyclic AMP and p38 mitogen-activated protein kinase

Mammalian genes coordinately regulated by growth arrest signals and DNA-damaging agents.

Cloning and functional analysis of the hematopoietic cell‐specific phospholipase Cγ² promoter

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Transcriptional inactivation of c-myc and the transferrin receptor in dibutyryl cyclic AMP-treated HL-60 cells.

Cited by 44 publications

References 28 publications

Involvement of fatty acid-CoA ligase 4 in hepatocellular carcinoma growth: Roles of cyclic AMP and p38 mitogen-activated protein kinase

Involvement of fatty acid-CoA ligase 4 in hepatocellular carcinoma growth: Roles of cyclic AMP and p38 mitogen-activated protein kinase

Mammalian genes coordinately regulated by growth arrest signals and DNA-damaging agents.

Cloning and functional analysis of the hematopoietic cell‐specific phospholipase Cγ2 promoter

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Cloning and functional analysis of the hematopoietic cell‐specific phospholipase Cγ² promoter