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We are analyzing https://link.springer.com/article/10.1007/s11596-009-0421-9.

Title:
Effects of 5-Aza-CdR on the proliferation of human breast cancer cell line MCF-7 and on the expression of Apaf-1 gene | Current Medical Science
Description:
Hypermethylation in the promoter region of tumor suppressor genes is a common mechanism of gene silencing, which tends to occur in cancer. The effects of 5-Aza-2β€²-deoxycytidine (5-Aza-CdR), a specific DNA methyltransferase inhibitor, on the cell proliferation of human breast cancer cell line MCF-7 and on the expression of Apaf-1 gene were investigated. Human MCF-7 cells were incubated with increasing concentrations of 5-Aza-CdR for 12 to 120 h. The growth inhibition rates of MCF-7 cells were detected by MTT assay. Changes of cell cycle distribution and apoptotic rates of MCF-7 cells were determined by flow cytometry. The expressions of DNA methyltransferase 3b mRNA and Apaf-1 mRNA were measured by reverse transcription polymerase chain reaction (RT-PCR). Meanwhile, the expression of Apaf-1 protein was detected by Western blotting. The results showed that 5-Aza-CdR significantly inhibited the growth of MCF-7 cells and the growth inhibition rate of MCF-7 cells was significantly enhanced with the concentration of 5-Aza-CdR and the action time. Flow cytometry indicated that 5-Aza-CdR could significantly induce G1/S cell cycle arrest and increase the apoptosis rate of MCF-7 cells. The mRNA and protein expressions of Apaf-1 were up-regulated in MCF-7 cells treated with 5-Aza-CdR, which was accompanied by down-regulation of DNA methyltransferase 3b mRNA. It is concluded that 5-Aza-CdR might retard the growth of tumor cells and promote the apoptosis of MCF-7 breast cancer cells by inhibiting the expression of DNA methyltransferase 3b and re-activating the Apaf-1 gene expression.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
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Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

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Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {πŸ’Έ}

We don't see any clear sign of profit-making.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {πŸ”}

article, google, scholar, cancer, pubmed, cas, cell, cells, gene, expression, apaf, mcf, azacdr, dna, breast, human, sci, effects, methyltransferase, methylation, huazhong, promoter, mrna, med, carcinoma, privacy, cookies, content, journal, proliferation, xiong, tumor, growth, apoptosis, access, publish, search, university, line, hypermethylation, suppressor, genes, azadeoxycytidine, apoptotic, kim, data, information, log, research, science,

Topics {βœ’οΈ}

month download article/chapter cadmium-induced malignant transformation tumor suppressor genes genome-wide gene expression dna methyltransferase 3b human mcf-7 cells related subjects full article pdf demethylating reagent 5-aza-2β€²-deoxycytidine 5-aza-cdr significantly inhibited mammary carcinoma cells privacy choices/manage cookies del principe mi 5-aza-cdr induced demethylation cell cycle distribution cell cycle arrest mammalian dna methyltransferases lovo cells induced mcf-7 cells treated biochem cell biol plakoglobin gene transcription tongji medical college mitochondrial apoptotic machinery palb2 susceptibility gene fhit gene contributes european economic area clin exp metastasis water-deprived rats consequent phenotypic conversion normal neural tissues environ health perspect apaf-1 gene published dna methyltransferase 1 dna methylation breast cancer conditions privacy policy significantly induce g1/ molecular targeted drugs provincial hospital affiliated tumor cells article journal article xiong differential apaf-1 levels check access instant access mrna expression profiles accepting optional cookies acute myeloid leukemia huazhong univ apaf-1 gene expression

Schema {πŸ—ΊοΈ}

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         headline:Effects of 5-Aza-CdR on the proliferation of human breast cancer cell line MCF-7 and on the expression of Apaf-1 gene
         description:Hypermethylation in the promoter region of tumor suppressor genes is a common mechanism of gene silencing, which tends to occur in cancer. The effects of 5-Aza-2β€²-deoxycytidine (5-Aza-CdR), a specific DNA methyltransferase inhibitor, on the cell proliferation of human breast cancer cell line MCF-7 and on the expression of Apaf-1 gene were investigated. Human MCF-7 cells were incubated with increasing concentrations of 5-Aza-CdR for 12 to 120 h. The growth inhibition rates of MCF-7 cells were detected by MTT assay. Changes of cell cycle distribution and apoptotic rates of MCF-7 cells were determined by flow cytometry. The expressions of DNA methyltransferase 3b mRNA and Apaf-1 mRNA were measured by reverse transcription polymerase chain reaction (RT-PCR). Meanwhile, the expression of Apaf-1 protein was detected by Western blotting. The results showed that 5-Aza-CdR significantly inhibited the growth of MCF-7 cells and the growth inhibition rate of MCF-7 cells was significantly enhanced with the concentration of 5-Aza-CdR and the action time. Flow cytometry indicated that 5-Aza-CdR could significantly induce G1/S cell cycle arrest and increase the apoptosis rate of MCF-7 cells. The mRNA and protein expressions of Apaf-1 were up-regulated in MCF-7 cells treated with 5-Aza-CdR, which was accompanied by down-regulation of DNA methyltransferase 3b mRNA. It is concluded that 5-Aza-CdR might retard the growth of tumor cells and promote the apoptosis of MCF-7 breast cancer cells by inhibiting the expression of DNA methyltransferase 3b and re-activating the Apaf-1 gene expression.
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            name:Journal of Huazhong University of Science and Technology [Medical Sciences]
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      headline:Effects of 5-Aza-CdR on the proliferation of human breast cancer cell line MCF-7 and on the expression of Apaf-1 gene
      description:Hypermethylation in the promoter region of tumor suppressor genes is a common mechanism of gene silencing, which tends to occur in cancer. The effects of 5-Aza-2β€²-deoxycytidine (5-Aza-CdR), a specific DNA methyltransferase inhibitor, on the cell proliferation of human breast cancer cell line MCF-7 and on the expression of Apaf-1 gene were investigated. Human MCF-7 cells were incubated with increasing concentrations of 5-Aza-CdR for 12 to 120 h. The growth inhibition rates of MCF-7 cells were detected by MTT assay. Changes of cell cycle distribution and apoptotic rates of MCF-7 cells were determined by flow cytometry. The expressions of DNA methyltransferase 3b mRNA and Apaf-1 mRNA were measured by reverse transcription polymerase chain reaction (RT-PCR). Meanwhile, the expression of Apaf-1 protein was detected by Western blotting. The results showed that 5-Aza-CdR significantly inhibited the growth of MCF-7 cells and the growth inhibition rate of MCF-7 cells was significantly enhanced with the concentration of 5-Aza-CdR and the action time. Flow cytometry indicated that 5-Aza-CdR could significantly induce G1/S cell cycle arrest and increase the apoptosis rate of MCF-7 cells. The mRNA and protein expressions of Apaf-1 were up-regulated in MCF-7 cells treated with 5-Aza-CdR, which was accompanied by down-regulation of DNA methyltransferase 3b mRNA. It is concluded that 5-Aza-CdR might retard the growth of tumor cells and promote the apoptosis of MCF-7 breast cancer cells by inhibiting the expression of DNA methyltransferase 3b and re-activating the Apaf-1 gene expression.
      datePublished:2009-08-07T00:00:00Z
      dateModified:2009-08-07T00:00:00Z
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External Links {πŸ”—}(95)

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