GSTM3 reverses the resistance of hepatoma cells to radiation by regulating the expression of cell cycle/apoptosis-related molecules

Sun, Ying; Wang, Yu; Yin, Yufeng; Xiang-hua, Chen; Sun, Zhi‐Jun

doi:10.3892/ol.2014.2358

Cited by 13 publications

(17 citation statements)

References 21 publications

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“…Following myocardial ischemia/reperfusion injury, enhanced apoptosis has been demonstrated [26]. Studies have indicated that upregulation of p27 significantly enhances cell apoptosis [27].In previous studies, regulation of p27 has been reported at different levels [10]. Alterations of cell cycle regulatory molecules play key roles in various diseases, such as cancer and cardiac injury [28].…”

Section: Discussionmentioning

confidence: 99%

Long Non Coding RNA-UCA1 Contributes to Cardiomyocyte Apoptosis by Suppression of p27 Expression

Liu

Daliang(²,

et al. 2015

Cell Physiol Biochem

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This is an Open Access article licensed under the terms of the Creative Commons AttributionNonCommercial 3.0 Unported license (CC BY-NC) (www.karger.com/OA-license), applicable to the online version of the article only. Distribution permitted for non-commercial purposes only. Key WordsLong non coding RNA • UCA1 • Cardiomyocyte apoptosis • p27 Abstract Background/Aims: Urothelial carcinoma-associated 1 (UCA1) is a recently identified long non coding RNA (lncRNA). However, few studies have explored its role in cardiomyocytes after focal cardiac ischemia reperfusion injury (CIR). Methods: Rat CIR models were established using ligation of the Lower Anterior Descending artery (LAD). Cell apoptosis and reactive oxygen species (ROS) production in cardiac tissues were explored using immunohistochemistry and DHE staining. lncRNA expression patterns were detected using microarray and validated by qPCR. Cell viability and apoptosis were examined using MTT assay and flow cytometry. Results: CIR significantly induced cell apoptosis and ROS production in the rat model. The results of microarray demonstrated the reduced expression of UCA1, which was validated by qPCR. Follow-up experiments showed that UCA1 was involved in H 2 O 2 -induced cell apoptosis. We further showed that UCA1 negatively correlated with the expression of p27. Moreover, overexpression of p27 could induce primary cardiomyocyte apoptosis. Conclusions: Reduction of UCA1 levels plays a pro-apoptotic role in primary cardiomyocytes partially through stimulation of p27 protein expression. These results are in agreement with the observed levels of UCA1, p27 and apoptosis after cardiac I/R injury, suggesting that UCA1 might have an important role during I/R injury.

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Section: Discussionmentioning

confidence: 99%

Long Non Coding RNA-UCA1 Contributes to Cardiomyocyte Apoptosis by Suppression of p27 Expression

Liu

Daliang(²,

et al. 2015

Cell Physiol Biochem

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“…Two of these eGenes, GSTM3 and HSPA6, are associated with diseases such as HBV for GSTM3 and HCC for both eGenes. [28][29][30][31] These are diseases that disproportionately affect African Americans. 32,33 GSTM3 has also been associated to oxidative stress and specifically several studies have found that epigenetic suppression of GSTM3 in HBV-infected cells causes oxidative stress 29,30 , which can lead to HCC.…”

Section: Discussionmentioning

confidence: 99%

“…[28][29][30][31] These are diseases that disproportionately affect African Americans. 32,33 GSTM3 has also been associated to oxidative stress and specifically several studies have found that epigenetic suppression of GSTM3 in HBV-infected cells causes oxidative stress 29,30 , which can lead to HCC. 28 Furthermore, other studies showed that GSTM3 expression was lowered with promoter hypermethylation 34 and in chemical-induced HCC.…”

Section: Discussionmentioning

confidence: 99%

“…Two of these eGenes, GSTM3 (FDR = 0.014) and HSPA6 (FDR = 0.029), have been associated to disease traits such as Hepatitis B (HBV) for GSTM3 and Hepatocellular Carcinoma (HCC) for both eGenes. [28][29][30][31] African Americans have a higher incidence and worse outcomes of HBV and HCC when compared to other demographics. 32,33 Since these eGenes were not significant with PC-adjusted eQTL mapping, they may explain how methylation plays a role in the health disparities observed in African Americans.…”

Section: Discovery Of Egenes Associated To Disease Traits Using Methymentioning

confidence: 99%

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Incorporation of DNA methylation into eQTL mapping in African Americans

Singh¹,

Zhong²,

Nahlawi³

et al. 2020

Preprint

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Epigenetics is a reversible molecular mechanism that plays a critical role in many developmental, adaptive, and disease processes. DNA methylation has been shown to regulate gene expression and the advent of high throughput technologies has made genome-wide DNA methylation analysis possible. We investigated the effect of DNA methylation in eQTL mapping (methylation-adjusted eQTLs), by incorporating DNA methylation as a SNP-based covariate in eQTL mapping in African American derived hepatocytes. We found that the addition of DNA methylation uncovered new eQTLs and eGenes. Previously discovered eQTLs were significantly altered by the addition of DNA methylation data suggesting that methylation may modulate the association of SNPs to gene expression. We found that methylation-adjusted eQTLs which were less significant compared to PC-adjusted eQTLs were enriched in lipoprotein measurements (FDR = 0.0040), immune system disorders (FDR = 0.0042), and liver enzyme measurements (FDR = 0.047), suggesting a role of DNA methylation in regulating the genetic basis of these phenotypes. Our methylation-adjusted eQTL analysis also uncovered novel SNP-gene pairs. For example, our study found the SNP, rs11546996, was associated to PNKP. In a previous GWAS, this SNP was associated with primary biliary cirrhosis although the causal gene was thought to be SPIB. Our methylation-adjusted method potentially adds new understanding to the genetic basis of complex diseases that disproportionally affect African Americans.

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“…The alpha-class Gsts have been reported to play an important role as antioxidant enzymes modulating stress-induced apoptosis pathways (Yang et al , 2001) and are associated with “immunity and defense” (Yun et al , 2009). Gstm3 regulates apoptosis- and proliferation-related pathways and was identified as a tumor suppressor (Sun et al , 2014), whereas theta-class Gsts (Gstt2 and 3) are critical in the early response induced by toxicants, such as D-galactosamine and 1-menaphthyl sulphate, due to altered oxidative stress (Coggan et al , 2002; Yun et al , 2010). Therefore, mice on the restricted diet, atherogenic diet, and lab chow might be more resistant to carcinogens and by-products of oxidative stress, compared to mice on the AIN-93M purified diet.…”

Section: Discussionmentioning

confidence: 99%

Effect of nine diets on mRNAs of phase-II conjugation enzymes in livers of mice

et al. 2016

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Phase-II enzymes are important in metabolizing many xenobiotics including prescription drugs and chemical carcinogens. Whereas it is known that diet can alter the expression of phase-II conjugation enzymes, the previous studies are limited in using only two or three diets and examining only a few enzymes.Adult male C57BL6 mice were fed one of 9 diets for 3 weeks. Of the 87 genes encoding major hepatic phase-II enzymes, approximately one-half (43) were altered by at least one diet. Diet restriction altered the hepatic expression of the most genes encoding phase-II enzymes (27), followed by lab chow (15), atherogenic diet (13), high-fat diet (10), western diet (7), high-fructose diet (5), and essential fatty acid-deficient diet (3), whereas the low n-3 fatty acid diet had no effect on the hepatic expression of these phase-II enzymes.This comprehensive study provides detailed information on which conjugation enzymes are changed by these diets, and these data can be used to further investigate the mechanism for these changes in messenger RNAs, and whether these changes result in alterations in enzyme activity and drug action.

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GSTM3 reverses the resistance of hepatoma cells to radiation by regulating the expression of cell cycle/apoptosis-related molecules

Cited by 13 publications

References 21 publications

Long Non Coding RNA-UCA1 Contributes to Cardiomyocyte Apoptosis by Suppression of p27 Expression

Long Non Coding RNA-UCA1 Contributes to Cardiomyocyte Apoptosis by Suppression of p27 Expression

Incorporation of DNA methylation into eQTL mapping in African Americans

Effect of nine diets on mRNAs of phase-II conjugation enzymes in livers of mice

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