Evaluation of methylation status in glutation S-transferase P1(GSTP1) gene promoter in human breast cancer and its relation to tumor grade and stage

2011 ◽  
Vol 6 (27) ◽  
Author(s):  
Shohreh Alizadeh Shargh,
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Methylation Status ◽  
Gene Promoter ◽  
Tumor Grade ◽  
Human Breast ◽  
Gstp1 Gene

Expression of inducible nitric oxide synthase in human breast cancer depends on tumor grade

1999 ◽  
Vol 56 (2) ◽  
pp. 143-149 ◽  
Author(s):  
Walter Tschugguel ◽  
Christian Schneeberger ◽  
Gertrud Unfried ◽  
Klaus Czerwenka ◽  
Wolfgang Weninger ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Human Breast Cancer ◽  
Tumor Grade ◽  
Human Breast ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

scholarly journals PKM2 in Canine Mammary Tumors: Parallels to Human Breast Cancer

2020 ◽  
Vol 70 (4) ◽  
pp. 349-354
Author(s):  
Hyo-Ju Lee ◽  
Hyo-Jeong Han ◽  
Ji-Young Lee ◽  
Woo-Chan Son
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Aerobic Glycolysis ◽  
Prognostic Significance ◽  
Tumor Grade ◽  
Mammary Tumors ◽  
Neoplastic Disease ◽  
Human Breast ◽  
Rate Limiting Step ◽  
Canine Mammary Tumors

PKM2 is a pyruvate kinase isoform that is the final and rate-limiting step in aerobic glycolysis in tumor cells. Increased expression of PKM2 has been detected in human cancers. The present study examined the expression of PKM2 in canine mammary tumors and assessed its prognostic significance. Paraffin sections of 5 adenomas, 67 carcinomas, and 5 samples of nonneoplastic hyperplasia from 77 dogs, aged 8 to 18 y, were evaluated. Significantly higher levels of PKM2 were detected among the carcinomas compared with all other tissues examined. The level of PKM2 expression in carcinoma tissue correlated positively with the tumor grade. These findings suggest that PKM2 may have a similar role in canine mammary tumors to its role in human breast cancer. As such, canine mammary tumors may be useful models for studies focused on the progression of human neoplastic disease.

Methylation status of the Ep-CAM promoter region in human breast cancer cell lines and breast cancer tissue

2007 ◽  
Vol 246 (1-2) ◽  
pp. 253-261 ◽  
Author(s):  
Gilbert Spizzo ◽  
Guenther Gastl ◽  
Peter Obrist ◽  
Dominic Fong ◽  
Margot Haun ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Cell ◽  
Promoter Region ◽  
Human Breast Cancer ◽  
Methylation Status ◽  
Human Breast Cancer Cell ◽  
Breast Cancer Tissue ◽  
Breast Cancer Cell Lines ◽  
Cancer Tissue ◽  
Human Breast

scholarly journals Mechanism of transcriptional regulation of LRP16 gene expression by 17-β estradiol in MCF-7 human breast cancer cells

2005 ◽  
Vol 34 (1) ◽  
pp. 77-89 ◽  
Author(s):  
Y-L Zhao ◽  
W-D Han ◽  
Q Li ◽  
Y-M Mu ◽  
X-C Lu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Promoter Region ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Gene Promoter ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
E Box ◽  
Mcf 7

LRP16 gene expression is induced by 17-βestradiol (E2) via estrogen receptor alpha (ERα) in MCF-7 human breast cancer cells. A previous study also demonstrated that ectopic expression of LRP16 gene promoted MCF-7 cell proliferation. To explore the mechanism of hormone-induced LRP16 gene expression, the LRP16 gene promoter region (−2600 to −24 bp upstream of the LRP16 gene translation starting site) was analyzed in the present study by using different 5′-truncated constructs, and a luciferase reporter. The 5′-flanking sequence of −676 to −24 bp (pGL3-S5) was found to be E2-responsive. After exchange of the fragment from −213 to −24 bp with the TK gene proximal promoter region in pGL3-S5, E2 still induced reporter gene activity in MCF-7 and HeLa cells. Sequence analysis showed that the pGL3-S6 (−676 to −214) sequence contains two motifs that may contribute to E2-induced transactivation; namely, an estrogen-responsive element (ERE) half-site/Sp1 at −246 to −227 bp and an E-box site at −225 to −219 bp. Further deletion and mutation analysis of these two motifs indicated that both the 1/2 ERE and Sp1 binding sites were required for E2 action, while E-box deletion did not affect the luciferase activity in MCF-7 and HeLa cells. The results of gel mobility shift and chromatin immunoprecipitation assays confirmed that both ERαand Sp1 were required for hormone-induced transactivation, which involved both ERαand Sp1 directly binding to DNA. Taken together, these findings suggest that ERαand Sp1 play a role in activation of the human LRP16 gene promoter.

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