ArticleKorean journal of anesthesiology2010
The expression of survivin and its related genes in adipocyte-derived stem cell by demethylation.
Article in Korean journal of anesthesiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Epidermal stem cells participate in the repair of scalds via Nanog and Myc regulation.Molecular medicine reports · 2022Article
- Emerging Importance of Survivin in Stem Cells and Cancer: the Development of New Cancer Therapeutics.Stem cell reviews and reports · 2020Review
- Transcription factor TCF4 maintains the properties of human corneal epithelial stem cells.Stem cells (Dayton, Ohio) · 2012Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSurvivin is thought to contribute to stem cell maintenance partly by a hypomethylation mechanism. This study attempted to elucidate the signal transduction pathway of adipocyte-derived stem cells (ASCs) by using a demethylating agent, 5-aza-2'-deoxycytidine (ADC), to analyze the survivin, MEK/ERK, c-Myc and p53 gene expression.
methodsDemethylation in the ASCs was induced by 1 microM ADC treatment. RT-PCR for survivin mRNA was preformed, before and 24, 48 and 72 hours (hr) after ADC treatment. Western blotting analysis was performed for p53, survivin, unphosphorylated and phosphorylated (p)-MEK, and p-ERK. Immunohistochemistry for ERK and survivin was done to evaluate the localization of the proteins.
resultsADC inhibited the population growth of the ASCs and it increased the number of apoptotic cells 24, 48, and 72 hr after treatment. ADC treatment slightly decreased the expression of survivin mRNA after 48 hr and its level was restored after 72 hr of treatment. Otherwise, the level of survivin protein gradually increased up to 48 hr and it was decreased at 72 hr. The levels of p-MEK and p53 were increased time-dependently. c-Myc and p-ERK were elevated after ADC treatment and their highest levels were seen 48 hr after treatment. The ADC treatment increased the nuclear expression of ERK and survivin in the ASCs.
conclusionsThe overexpression of p-MEK/ERK, p53, and c-Myc increased the survivin protein expression of the demethylated ASCs. These results suggest that demethylation could alter the expression of survivin, and p53, c-Myc and the MAPK (MEK/ERK) pathway might play a role in survivin's regulation in ASCs.
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Registered trials
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