scholarly journals Analysis of mRNA expression and DNA methylation level of RAC1 gene encoding focal adhesion molecule in endometrial and peritoneal endometriosis

2020 ◽  
pp. 43-49
Author(s):  
Irwina Eka Deraya ◽  
Andon Hestiantoro ◽  
Raden Muharam ◽  
Muhammad Lucky Marwali ◽  
Agus Surur As'adi ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Mrna Expression ◽  
Focal Adhesion ◽  
Methylation Level ◽  
Promoter Hypermethylation ◽  
Mrna Expression Level ◽  
Normal Endometrium ◽  
Significant Difference ◽  
Its Gene ◽  
Peritoneal Endometriosis

Focal adhesion molecules involve in cellular migration, attachment, and play a role in endometriosis pathomechanisms. Recent studies showed that the expression of RAC1, a gene encoded focal adhesion molecule, was predominantly found in endometriosis. As gene expression may be regulated by DNA methylation. Therefore, this study aimed to analyze promoter methylation level of RAC1 gene and mRNA expression in endometrial and peritoneal endometriosis tissues. This study using 20 endometrial and 9 peritoneal tissues from the same patients and 20 normal endometrial. The DNA and RNA from samples were isolated, DNA was converted using sodium bisulfite and amplified using Methyl Specific Polymerase Chain Reaction (MSP) method. The methylation level was determined by the intensity measurement of the bands that arose in gel electrophoresis using ImageJ software, whereas mRNA expression level was measured by Reverse Transcription-quantitative PCR (RT-qPCR) method. The mRNA expression level of RAC1 gene in peritoneal endometriosis increased compared to normal endometrium, as well as compared to endometrial endometriosis, but there was no significant difference in endometrial endometriosis compared to normal. Promoter hypermethylation level of RAC1 gene in peritoneal endometriosis was significantly different compared to normal endometrium, however not significant to endometrial endometriosis. Methylation level of its gene in endometrial endometriosis shown no significant difference compared to normal. There was association between promoter hypermethylation level and its mRNA expression in endometrial endometriosis (R= 0.014; p=0.952). The elevation of mRNA expression of RAC1 gene plays a role in endometrial cell migration to peritoneum, and associated with promoter hypermethylation level of its gene.

scholarly journals Analysis of DNA methylation level and mRNA expression of Transient Receptor Ankyrin Member 1 (TRPA1) in endometriosis-associated pain

2021 ◽  
pp. 1-10
Author(s):  
Ocktariyana ◽  
Nurul Hikmawati ◽  
Andon Hestiantoro ◽  
Raden Muharam ◽  
Muhammad Luky Marwali ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Mrna Expression ◽  
Methylation Level ◽  
Rating Scale ◽  
Expression Level ◽  
Pain Level ◽  
Mrna Expression Level ◽  
Significant Difference ◽  
Peritoneal Endometriosis ◽  
Transient Receptor

Transient Receptor Ankyrin Member 1 (TRPA1) is an ion channel family protein that regulates pain sensation through sensory neurons' activity. This study's purpose to analyzes the DNA methylation and mRNA expression level of the TRPA1 gene in endometriosis and its correlation with pain level. Twenty samples of peritoneal endometriosis and endometrial samples were obtained from women with endometriosis, which was subsequently compared to 20 endometrial samples of women without endometriosis. The DNA methylation level of TRPA1 was analyzed using Methylation-specific PCR (MS-PCR) and ImageJ software, while the mRNA expression of TRPA1 was analyzed using qRT-PCR. Furthermore, the pain level was measured using the numeric rating scale (NRS) by interviewing all the women. This study showed that there was a significant difference in the mRNA expression of TRPA1 in peritoneal endometriosis. The TRPA1 was unmethylated in both peritoneal and endometrial samples in endometriosis. However, DNA Methylation level of TRPA1 in peritoneal and endometrial of endometriosis compared to normal endometrial were no significant difference. Additionally, there was no correlation between DNA methylation level and mRNA expression level of TRPA1 in all samples, along with the endometriosis-associated pain.

ATF4, DLX3, FRA1, MSX2, C/EBP-ζ, and C/EBP-α Shape the Molecular Basis of Therapeutic Effects of Zoledronic Acid in Bone Disorders

2020 ◽  
Vol 20 (18) ◽  
pp. 2274-2284
Author(s):  
Faroogh Marofi ◽  
Jalal Choupani ◽  
Saeed Solali ◽  
Ghasem Vahedi ◽  
Ali Hassanzadeh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Zoledronic Acid ◽  
Mrna Expression ◽  
Promoter Methylation ◽  
Methylation Level ◽  
Target Genes ◽  
Osteoblastic Differentiation ◽  
Therapeutic Effects ◽  
Significant Difference ◽  
Scheduled Time

Objective: Zoledronic Acid (ZA) is one of the common treatment choices used in various boneassociated conditions. Also, many studies have investigated the effect of ZA on Osteoblastic-Differentiation (OSD) of Mesenchymal Stem Cells (MSCs), but its clear molecular mechanism(s) has remained to be understood. It seems that the methylation of the promoter region of key genes might be an important factor involved in the regulation of genes responsible for OSD. The present study aimed to evaluate the changes in the mRNA expression and promoter methylation of central Transcription Factors (TFs) during OSD of MSCs under treatment with ZA. Materials and Methods: MSCs were induced to be differentiated into the osteoblastic cell lineage using routine protocols. MSCs received ZA during OSD and then the methylation and mRNA expression levels of target genes were measured by Methylation Specific-quantitative Polymerase Chain Reaction (MS-qPCR) and real.time PCR, respectively. The osteoblastic differentiation was confirmed by Alizarin Red Staining and the related markers to this stage. Results: Gene expression and promoter methylation level for DLX3, FRA1, ATF4, MSX2, C/EBPζ, and C/EBPa were up or down-regulated in both ZA-treated and untreated cells during the osteodifferentiation process on days 0 to 21. ATF4, DLX3, and FRA1 genes were significantly up-regulated during the OSD processes, while the result for MSX2, C/EBPζ, and C/EBPa was reverse. On the other hand, ATF4 and DLX3 methylation levels gradually reduced in both ZA-treated and untreated cells during the osteodifferentiation process on days 0 to 21, while the pattern was increasing for MSX2 and C/EBPa. The methylation pattern of C/EBPζ was upward in untreated groups while it had a downward pattern in ZA-treated groups at the same scheduled time. The result for FRA1 was not significant in both groups at the same scheduled time (days 0-21). Conclusion: The results indicated that promoter-hypomethylation of ATF4, DLX3, and FRA1 genes might be one of the mechanism(s) controlling their gene expression. Moreover, we found that promoter-hypermethylation led to the down-regulation of MSX2, C/EBP-ζ and C/EBP-α. The results implicate that ATF4, DLX3 and FRA1 may act as inducers of OSD while MSX2, C/EBP-ζ and C/EBP-α could act as the inhibitor ones. We also determined that promoter-methylation is an important process in the regulation of OSD. However, yet there was no significant difference in the promoter-methylation level of selected TFs in ZA-treated and control cells, a methylation- independent pathway might be involved in the regulation of target genes during OSD of MSCs.

scholarly journals DNA methylation and retinal degenerative diseases: at the crossroad between genes and diet

2020 ◽  
Vol 53 (383) ◽  
pp. MISC1-MISC3
Author(s):  
Andrea Maugeri
Keyword(s):  
Dna Methylation ◽  
Methylation Level ◽  
Integrated Approach ◽  
Dietary Factors ◽  
Epigenetic Mechanisms ◽  
Degenerative Diseases ◽  
Retinal Cells ◽  
Significant Difference ◽  
Retinal Degenerative Diseases ◽  
The Impact

Retinal degenerative diseases are the leading causes of blindness and low vision among working-age and older adults worldwide, with 170 and 130 million individuals suffering from age-related macular degeneration (AMD) and diabetic retinopathy, respectively. Although several studies began to show benefits from dietary interventions against retinal degenerative disease, an integrated approach is needed to understand molecular mechanisms underpinning the protective or risky effect of dietary factors. A specific area of research that elucidates mechanisms involved in gene-diet interaction is the Nutri-epigenomics, the study of the impact of diet on gene expression by modulating epigenetic mechanisms. The present research investigated the role of DNA methylation – one of the most commonly analysed epigenetic mechanisms - in the pathophysiology of retinal degenerative diseases, by exploiting a multiple integrated approach. In vitro studies initially helped us to understand how pathological features of retinal degeneration (e.g. oxidative stress, inflammation and hyperglycaemia) modulated functions of enzymes involved in the methylation of Long Interspersed Nuclear Element 1 (LINE-1) sequences in retinal cells. We also proved that some nutrients (e.g. resveratrol and curcumin) might counteract these effects and restore DNA methylation level in retinal cells under oxidative, inflammatory and high glucose conditions. We further analysed whether LINE-1 methylation level differed between patients with AMD and controls without posterior segment eye diseases. Interestingly, we noted a significant difference between the two groups, with higher LINE-1 methylation level in blood samples from AMD patients. This evidence -albeit promising for biomarker discovery- requires confirmation by further large-size prospective studies taking into account different factors. Our research, in fact, also suggested that the risk of retinal degenerative diseases derives from the combination of genetic risk variants, clinical characteristics, environmental exposures and unhealthy lifestyles, which in turn are interrelated. Thus, it would be interesting to study how the exposome -the totality of exposures individuals experience over the course of life- might induce epigenetic mechanisms able to reduce or increase the risk for retinal degenerative diseases.

scholarly journals PSIV-B-38 Late-Breaking: Effect of Glutamate (Glu) on Developmental Block and the MZT Relative Genes Expression in Mouse embryo during in Vitro Culture

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 330-331
Author(s):  
Yu Liu ◽  
An Gang Lou ◽  
Shuo Yang ◽  
Zhong Shu Li ◽  
Nan-Zhu Fang
Keyword(s):  
In Vitro Culture ◽  
Mrna Expression ◽  
Marker Gene ◽  
Treated Group ◽  
Mouse Embryos ◽  
Expression Level ◽  
Mrna Expression Level ◽  
Significant Difference ◽  
Developmental Block

Abstract The risk of developmental block in mammal’s embryos is high during in vitro as compare to in vivo environment because the in vitro embryo-culture systems are suboptimal. During in vitro-culture the balance between ROS production and elimination is disturbed and may lead to 2-cell block in mouse embryos [1]. In the current study, we investigated the effects of Glu as anti-developmental block during IVC on ZGA and MZT on mouse embryos. The mouse embryos were divided into control and different level of Glu treated group. The cleavage rate was determined, the ROS and GSH level was investigated using DCHF-DA and CMF2HC respectively. The mRNA expression level of ZGA marker gene such as Eif-1α, Muerv l, Zscan4d and Hsp70.1 was analyzed among the groups using RT-PCR. The transition rate from 2-cell to 4-cell was significantly higher in 6mmol/L Glu treated group as compare to control and others treated groups. No significant difference was recorded in the level of ROS and GSH during MZT stage among the different groups. The mRNA expression level of ZGA marker gene was significantly increased at middle and late stage in 6mmol/L Glu treated group as compare to control and others treated groups. In conclusion, this study shows that the concentration of 6mmol/L Glu could maintain the dynamic balance of GSH and ROS, increase the expression of ZGA marker gene and maintain its high expression pattern of time series, directly participate in the ZGA activated process; ultimately reduce the risk of developmental block to ensure the successful completion of MZT. Reference [1] Lee MT, Bonneau AR, Giraldez AJ.Zygotic Genome Activation during the Maternal-to-Zygotic Transition. Annual Rev Cell Dev Biol [J], 2014, 30:581–613.

The Regulation of β-arrestin1 in Leukemia Initiating Cells of Children B-Acute Lymphoblastic Leukemia

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 3538-3538
Author(s):  
Lin Zou ◽  
Shan Liu ◽  
Yi Shu ◽  
Ru Qin ◽  
Kang Li ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Mrna Expression ◽  
Promoter Region ◽  
Lymphoblastic Leukemia ◽  
The Self ◽  
Mrna Expression Level ◽  
Self Renewal ◽  
Nsg Mice

Abstract Background Leukemia is the most common malignant tumor in children under 15 years old. The main subtype of children leukemia is acute lymphoblastic leukemia (ALL), and B-lineage ALL (B-ALL) accounts for approximately 70%. The leukemia-initiating cells (LICs) are cancer stem cells with long-term repopulating potential and propagation ability, to maintain the leukemia cell phenotype, and possess leukemia-initiating activity. However, the regulation of LICs for the leukemia progression is poorly understood. The multifunctional scaffold proteins β-arrestins are proven to mediate H4 acetylation and gene expression. And β-arrestin2 is found to regulate the initiation and progression of chronic myeloid leukemia (CML). However, the role of β-arrestin1 in B-ALL is still unknown. Our preliminary data showed that both the high expression of β-arrestin1 and high proportion of CD34+CD38- cells are positively correlated with risk stratification and poor prognosis of childhood B-ALL. And β-arrestin1 binds with EZH2 to increase BCR/ABL H4 acetylation and thus promotes CML cell progression in vitro and in vivo. The aim of study is to investigate the essential function of β-arrestin1 in LICs from B-ALL. Materials and Methods The bone marrow (BM) and periphery blood (PB) of children B-ALL patients were collected, isolated and identified LICs by Magnetic-activated cell sorting (MACS) and flow cytometry. The total RNA and protein were purified for gene and protein expression by real-time RT-PCR and Western blot. The leukemia cells (LICs, Raji, and Reh) of β-arrestin1 depletion were constructed by transient or stable screening si-β-arrestin1 (siβ1) lentivirus vector. The serial cell colony formation and NSG mice survival analysis was measured the LICs self-renewal ability. The CCK8 and MTS assays were used to detect the cell proliferation, and annexin V-FITC and PI staining for cell apoptosis. The DNA methylation of gene promoter region was detected by methylation-specific PCR and the methltransferase activity by ELISA. The telomere length was indicated by Southern blot and FISH, and telomerase activity by TRAP. Electrophoretic mobility shift assay (EMSA) and dual-luciferase reporter assay were applied to explain gene transcription. Student’s t test and Log-Rank test were used in the corresponding statistical significance and P<0.05 were considered significant. All the statistical analysis was performed using the GraphPad Prism (Version 5.0) software packages and SPSS 17.0. Results The expression of β-arrestin1 was elevated in LICs from B-ALL patients, and the high level of β-arrestin1 was negatively correlated with the survival of these patients. Further study showed that the loss of β-arrestin1 in B-ALL LICs attenuates their self-renewal capacity and promotes their senescence in vitro and in vivo. The mRNA expression level of β-arrestin1 is negatively correlated with that of PTEN in LICs. Moreover, the DNA methylation of the PTEN promoter region, the activity and the expression of DNMTs were enhanced in the LICs. The inhibition of DNMT1 activity impaired the self-renewal and increased the expression of PTEN of LICs. In addition, depletion of β-arrestin1 significantly decreased DNMT1 activity and PTEN methylation, and consistently increased PTEN expression in LICs. For B-ALL cell senescence, the mRNA expression level of β-arrestin1 is negatively related with the length of telomere, positively related with the activity of telomerase and the mRNA expression of hTERT in B-ALL LICs and engrafted NSG mice. Moreover, the weakened effect of β-arrestin1 on telomere, telomerase and the gene of hTERT were observed by injected the inhibitor of telomerase in leukemic mice. In addition, depletion of β-arrestin1 significantly decreased the binding of SP1 to the promoter of hTERT and thus reduced the transcription of hTERT in B-ALL Raji and Reh cells. Furthermore, β-arrestin1 interacted with P300 to bind with SP1 in the -104bp to -113bp of hTERT core promoter region in B-ALL cells. Conclusions β-arrestin1 could regulate the self-renewal and senescence of LICs from B-ALL, by partially mediating DNMT1 activity and hTERT transcription respectively, indicating that β-arrestin1 is a potential therapeutic target for B-ALL. Disclosures No relevant conflicts of interest to declare.

195 EFFECTS OF GSK3 INHIBITOR ON THE PLURIPOTENCY MAINTENANCE OF BUFFALO EMBRYONIC STEM-CELL-LIKE CELLS

2014 ◽  
Vol 26 (1) ◽  
pp. 212 ◽  
Author(s):  
F. Lu ◽  
Y. Lao ◽  
H. Sun ◽  
C. Lei ◽  
Y. Deng ◽  
...  
Keyword(s):  
Stem Cell ◽  
Embryonic Stem Cell ◽  
Mrna Expression ◽  
Colony Formation ◽  
Embryonic Stem ◽  
Signalling Pathway ◽  
Expression Level ◽  
Control Group ◽  
Mrna Expression Level ◽  
Significant Difference

In this study, to explore the effects and mechanism of Wnt/β-catenin signalling pathway on the maintenance of pluripotency of buffalo embryonic stem-cell-like cells (buffalo ESC-like cells), the GSK3 inhibitors BIO and CHIR99021 were added throughout the experiment – i.e. from buffalo inner cell mass (ICM) culture to ESC-like line generation. The buffalo ICM were respectively cultured in the medium containing 0.5 μg mL–1 BIO and 5 mmol L–1 CHIR99021. The percentage of ICMs attachment and primary colony formation were observed, and found that there was no significant difference in the ICMs attachment rate among of the BIO, CHIR99021, and the control groups (91.18% and 92.98% v. 94.59%; P > 0.05). Treating ICMs with CHIR99021 resulted in more primary colony formation rate compared with the control group (77.71% v. 55.41%; P < 0.05). The proliferation rate of primary colonies of buffalo ESC-like cells was detected by bromodeoxyuridine immunofluorescence techniques. The results show that the proliferation rate of primary colonies in the group of buffalo ESC-like cells treated with CHIR99021 was significantly higher than that of the control group on Day 1, Day 3, Day 4, and Day 5 (P < 0.05), and it was also evidently higher than that of control group only on Day 1 (P < 0.05) in the group of BIO, but there was no significant difference in other days (P > 0.05). The mRNA expression level of proliferation marker PCNA of ESC-like cells was significantly up-regulated in both CHIR99021 and BIO treatment groups (P < 0.05), however, treating buffalo ESC-like cells with CHIR99021 significantly up-regulated the expression of pluripotent gene Oct4 and Sox2 (P < 0.05), but had no effect on pluripotent gene Nanog expression (P > 0.05). Oct4 expression was significantly increased (P < 0.05), and the expression of Sox2 and Nanog were significantly decreased (P < 0.05) in the group of BIO treatment. Furthermore, the relative protein level of β-catenin (the downstream effector of Wnt/β-catenin signalling pathway) and the mRNA expression level of c-Myc (the downstream target gene of Wnt/β-catenin signalling pathway) were significantly increased when buffalo ESC-like cells respectively treated with CHIR99021 and BIO (P < 0.05). In conclusion, treating buffalo ESC-like cells with GSK3 inhibitors CHIR99021 can promote proliferation of buffalo ESC-like cells, maintain their undifferentiated state, and up-regulate the expression levels of β-Catenin and c-Myc in buffalo ESC-like cells. These results indicate that Wnt/β-catenin signalling pathway plays an important role in regulation of self-renewal of buffalo ESC-like cells. This work was funded by the China High Technology Development Program (2011AA100607), China Natural Science Foundation (31072033), and Guangxi Science Foundation (2012GXNSFFA060004).

scholarly journals THU0024 METHYLATION ANALYSIS OF VITAMIN D SIGNALING PATHWAY GENES IN RHEUMATOID ARTHRITIS PATIENTS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 225.1-225
Author(s):  
E. Punceviciene ◽  
J. Gaizevska ◽  
R. Sabaliauskaite ◽  
L. Venceviciene ◽  
D. Vitkus ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Dna Methylation ◽  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Methylation Level ◽  
Methylation Pattern ◽  
Healthy Controls ◽  
Methylation Analysis ◽  
Vitamin D Metabolism ◽  
Significant Difference

Background:Vitamin D is known for its immunomodulatory and epigenome interacting effects. Vitamin D deficiency is frequently observed in rheumatoid arthritis (RA) patients compared to healthy controls, is also named as a potential risk factor in RA ethiopatogenesis and may alter DNA methylation of certain genes [1,2]. Still, causality of vitamin D deficiency in RA patients needs to be elucidated.Objectives:The aim of the study was to evaluate relationship between DNA methylation status of vitamin D related genes (VDR,CYP24A1,CYP2R1), miRNA-155 expression, vitamin D level and its association with RA.Methods:CpG islands in promoter region of theVDR,CYP24A1,CYP2R1genes were chosen for DNA methylation analysis by means of pyrosequencing. DNA from blood mononuclear cells of 31 RA patients and 31 age and sex matched healthy controls was assessed for methylation pattern after informed consent was obtained in Vilnius university Hospital Santaros klinikos Centre of Rheumatology. For miRNA analysis quantitative reverse transcription PCR was used. Chemiluminescent microplate immunoassay was used to asses 25(OH)D serum levels.Results:25(OH)D concentrations varied from deficiency (<50 nmol/l), insufficiency (50-75 nmol/l) to normal range (≥75-100 nmol/l) in RA (mean 47.49 nmol/l; SD ± 27.93) and healthy controls (mean 57.38 nmol/l; SD ± 29.93)).CYP24A1methylation level was significantly higher in comparison toVDR(p<0.0001) andCYP2R1(p<0.0001) genes in both groups.CYP24A1hypermethylation was also observed in older subjects (p=0.012). The study demonstrated a significant positive correlation between vitamin D concentration andVDR,CYP2R1genes methylation intensity (r2=0.31, p=0.014; r2=0.25, p=0.042, respectively). However, gene methylation frequency and methylation intensity showed no significant difference between RA patients and healthy controls (VDR– 2.4vs2.6 %,CYP24A1– 16.6vs15.3 %,CYP2R1– 2.6vs2.6 %) (p>0.05). To note, miRNA-155 expression negatively correlated withCYP24A1methylation intensity (r2=-0.43, p=0.009).Conclusion:Our study identified significant associations between theVDRandCYP2R1promoter methylation and vitamin D concentration. However, no significant differences in DNA methylation pattern between RA patients and healthy controls were detected. MiR-155 expression was associated withCYP24A1methylation level, confirming its possible involvement in vitamin D metabolism. The data of our study suggests that epigenetic phenomena are significantly involved in vitamin D metabolism and may have an indirect effect on RA ethiopatogenesis.References:[1]Jeffery LE, et al. Nat Rev Rheumatol. 2016,12.4:201.[2]Fetahu IS et al. Front Physiol. 2014,5:164.Acknowledgments:This project has received funding from the Research Council of Lithuania (LMTLT), agreement No. S-MIP-17-12.Disclosure of Interests:None declared

scholarly journals Regulation of RUNX3 expression by DNA methylation in prostate cancer

2020 ◽  
Author(s):  
Xin Yang ◽  
Shumei Wang ◽  
Alimu Reheman
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
Dna Methylation ◽  
Western Blot ◽  
Cell Lines ◽  
Methylation Level ◽  
Aberrant Methylation ◽  
Normal Prostate ◽  
Qrt Pcr ◽  
Its Gene

Abstract Background: Runt-related transcription factor 3 (RUNX3) is a developmental regulator, and methylation of the RUNX3 is significantly associated with the occurrence and development of carcinogenesis. Previous studies have identified an association of increased methylation level of RUNX3 in prostate cancer (PCa); however, the role and molecular mechanism underlying aberrant methylation of the RUNX3 gene in prostate tumorigenesis remain elusive. In this study, we will investigate the role of RUNX3 promoter methylation and its gene expression in PCa cells. Methods: The methylation of the RUNX3 in the promoter region in PCa cells was detected by bisulfite-sequencing PCR (BSP). Following treatment of the PCa cells with DNA methylation transferase inhibitor 5-AZA-2'-deoxycytidine (AZA), the effect on methylation level and expression of RUNX3 were analyzed by qRT-PCR, Western blot, and BSP assays. Furthermore, we investigated the effect of the demethylated RUNX3 on proliferation, cell cycle and apoptosis of PCa cells using CCK-8 and flow cytometry assays. Using the DNA methylation transferase (DNMT3b) knockout or overexpression models, the relationship between DNMT3b and RUNX3 methylation was further assessed by qRT-PCR, Western blot and methylation-specific PCR (MSP). Results: The results indicated that the methylation level of RUNX3 in PCa cell lines was significantly higher than that of normal prostate epithelial (RWPE-1) cells. Furthermore, treatment with AZA not only promoted the demethylation of RUNX3 but also restored the mRNA and protein expression of RUNX3, and the reactivation of expression of the later exhibited its anti-tumor effects through regulation of the cycle progression in PCa cells. Moreover, DNMT3b could regulate the expression level of RUNX3 by altering the DNA methylation of the RUNX3 in PCa cells. Conclusion: RUNX3 is hypermethylated in a panel of PCa cell lines; Inhibits DNA methylation of RUNX3 could restored its gene expression, which in turn induced its anti-cancer effects. Thus, RUNX3 may serve as a novel putative molecular target gene for PCa therapy.

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