Cloning and characterization of a human c-myc promoter-binding protein.

Ray, Ratna B.; Miller, Donald M.

doi:10.1128/mcb.11.4.2154

Cited by 107 publications

(131 citation statements)

References 69 publications

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“…1). A similar analysis with two other unrelated cellular genes, MBP-1 (Ray & Miller, 1991) and PTEN (Li et al, 1997), cloned into pcDNA3 vector did not suggest a detectable modulation of the p21 promoter activity (data not shown). Hepatocellular carcinoma accounts for over 90 % of primary liver cancers and may progress through inactivation of the p53 gene (Hsu et al, 1991).…”

mentioning

confidence: 79%

Hepatitis C virus NS5A protein modulates cell cycle regulatory genes and promotes cell growth.

Ghosh

Steele

Meyer

et al. 1999

Journal of General Virology

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confidence: 79%

Hepatitis C virus NS5A protein modulates cell cycle regulatory genes and promotes cell growth.

Ghosh

Steele

Meyer

et al. 1999

Journal of General Virology

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164

124

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“…The cell adhesion regulator gene is located at 16q24.3, within the distal region of common loss. In addition to the cell adhesion molecule genes, that for c-myc promoter-binding protein, which regulates the expression of the c-myc oncogene, is also located at 16q24 (Ray and Miller, 1991). The gene HSD17B2, located at 16q24.1-q24.2, is also a gene of interest.…”

Section: Discussionmentioning

confidence: 99%

“…The genes of two members of the cadherin superfamily, M-cadherin and H-cadherin, are located at 16q24 (Kaupman et al, 1992;Lee, 1996) and the expression of Hcadherin has been reported to be decreased in breast tumours (Lee, 1996). C-myc promoter-binding protein, whose gene is another possible target, is located at 16q24 and it is a negative regulator of c-myc oncogene expression (Ray and Miller, 1991).…”

mentioning

confidence: 99%

Three independently deleted regions at chromosome arm 16q in human prostate cancer: allelic loss at 16q24.1–q24.2 is associated with aggressive behaviour of the disease, recurrent growth, poor differentiation of the tumour and poor prognosis for the patient

et al. 1998

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Prostate cancer is one of the most common cancers among men in many Western countries, including Finland. However, the molecular genetic events associated with the development and progression of the disease are poorly known. According to the multistep model of carcinogenesis, several genetic aberrations take place in prostate cancer, but only a few genes potentially involved in prostatic carcinogenesis have been identified.It has been suggested that genetic alterations take place in several chromosomal regions in prostate cancer and, in comparative genomic hybridization (CGH) studies, the long arm of chromosome 16 is among those showing the most frequent loss (Joos et al, 1995;Visakorpi et al, 1995;Cher et al, 1996). Losses at chromosome 16 have been reported to occur almost exclusively in the long arm (q) (Bergerheim et al, 1991;Visakorpi et al, 1995;Cher et al, 1996). Both primary and metastatic tumours have been found to show allelic loss at 16q, and the occurrence of loss of heterozygosity (LOH) has also been associated with clinicopathological variables such as aggressive and metastatic behaviour of the disease and poor differentiation of the tumour (Carter et al, 1990;Suzuki et al, 1996;Elo et al, 1997;Latil et al, 1997). The most common area of deletion has been suggested to be distal in 16q, but the most recent results have indicated evidence of loss of several independent regions in 16q (Suzuki et al, 1996;Elo et al, 1997;Latil et al, 1997).Particular interest in losses at 16q has been paid to the region 16q21.1, where a potential tumour-suppressor gene, that for Ecadherin, is located. Decreased E-cadherin expression has been associated with poor prognosis of prostate cancer (Umbas et al, 1994). Recently, the regions of loss at chromosome arm 16q have been narrowed down. It has been suggested in several reports that losses at 16q are concentrated in three independent regions (Suzuki et al, 1996;Latil et al, 1997). The proximal area of loss is suggested to be located somewhere at 16q21.1 and the distal area of loss has been suggested to lie at 16q24.3. The central region of loss has been reported to be at 16q23.2 (Latil et al, 1997), but it has also been reported to be located at 16q23.2-q24.1 (Suzuki et al, 1996). Our recent data indicate that a 7.6-cM central area of loss is located at 16q24.1-q24.2, between markers D16S504 and D16S422. In addition, LOH at 16q24.1-q24.2 (HSD17B2 and D16S422) was found to be the most frequent area of deletion, and it was significantly correlated with aggressive and metastatic behaviour of the disease and also with poorly differentiated tumours (Elo et al, 1997).There are several candidate genes putatively involved in prostatic carcinogenesis located distally at 16q. The 17HSD type 2 gene (HSD17B2), located at 16q24.1-q24.2, encodes the 17β-hydroxysteroid dehydrogenase (17HSD) type 2 isoenzyme, which Summary Loss of heterozygosity at chromosome arm 16q is a frequent event in human prostate cancer. In this study, loss of heterozygosity at 16q was studied in 44 prostate ca...

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“…DENND4A, also known as C-myc promoter-binding protein MBP-1, acts as a general transcriptional repressor (35). It binds to c-myc promoter sequences and transcriptionally represses the c-myc gene (36)(37)(38). It has been demonstrated that overexpression of the MBP-1 gene induces apoptosis in several types of cancer cell line (39).…”

Section: Discussionmentioning

confidence: 99%

BMI-1 is important in bufalin-induced apoptosis of K562 cells

Lian

Wang

Wei

et al. 2014

Molecular Medicine Reports

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Abstract. The purpose of this study was to analyze the effects of bufalin on the gene expression of K562 cells and on the expression of BMI-1 pathway constituents in K562 cell apoptosis. K562 cells were treated with bufalin, and the inhibition rate and apoptosis were detected by an MTT assay, flow cytometry and a microarray assay. BMI-1, p16 INK4a and p14 ARF were examined by quantitative polymerase chain reaction (qPCR). Bufalin induced significant changes in the gene expression of the K562 cells; 4296 genes were differentially expressed, 2185 were upregulated and 2111 were downregulated. The most upregulated genes were associated with transcription regulation, while the most downregulated genes were associated with the non-coding RNA metabolic processes and DNA repair. qPCR analysis demonstrated that BMI-1 was overexpressed in the K562 cells. Bufalin is able to downregulate BMI-1 expression levels in K562 cells prematurely and cause an increase in the expression levels of p16 INK4a and p14 ARF . Moreover, bufalin downregulated BCR/ABL expression levels in a time-dependent manner, and the expression of BCR/ABL was not associated with the upregulation or downregulation of BMI-1 expression. Bufalin may induce K562 cell apoptosis by downregulating BMI-1 expression levels and accordingly upregulating the expression levels of p16 INK4a and p14 ARF . Bufalin may also induce K562 cell apoptosis via downregulating BCR/ABL expression levels, and this pathway may be independent of the BMI-1 pathway.

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Cloning and characterization of a human c-myc promoter-binding protein.

Cited by 107 publications

References 69 publications

Hepatitis C virus NS5A protein modulates cell cycle regulatory genes and promotes cell growth.

Hepatitis C virus NS5A protein modulates cell cycle regulatory genes and promotes cell growth.

Three independently deleted regions at chromosome arm 16q in human prostate cancer: allelic loss at 16q24.1–q24.2 is associated with aggressive behaviour of the disease, recurrent growth, poor differentiation of the tumour and poor prognosis for the patient

BMI-1 is important in bufalin-induced apoptosis of K562 cells

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