Publications by authors named "Reyhan Tahtasakal"

5 Publications

  • Page 1 of 1

MicroRNA profiling identifies Forkhead box transcription factor M1 (FOXM1) regulated miR-186 and miR-200b alterations in triple negative breast cancer.

Cell Signal 2021 Mar 18;83:109979. Epub 2021 Mar 18.

Center for RNA Interference and Non-Coding RNA, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address:

Breast cancer (BC) is the most commonly diagnosed malignancy. MicroRNAs (miRNAs) play important roles in the tumorigenesis, metastasis and progression of BC. Forkhead Box M1 (FOXM1) oncogenic transcription factor is involved in events considered as hallmarks of cancer. However, the specific mechanism by which FOXM1 exerts its oncogenic effects remains unclear and little is known about its effects on the regulation of miRNA expression. We have found that FOXM1 is upregulated in breast cancer cells and that its expression is associated with shortened overall survival and poor prognosis in patients with BC. Using microarray technology, we assessed the expression profiles of 752 miRNAs in highly aggressive and metastatic triple negative breast cancer (TNBC) cells in response to FOXM1 knockdown and identified 13 differentialy expressed miRNAs (3 miRNAs upregulated and 10 miRNAs down-regulated). We validated the results of the miRNA expression profile in two different TNBC cells by performing qRT-PCR and identified that miR-186-5p and miR-200b-5p were consistently down- or up-regulated, respectively, after knockdown of FOXM1. We further performed KEGG pathway analysis and GO enrichment analysis for miR-186-5p and miR-200b-5p, and identified that these miRNAs are associated with cancer development and progression involving toll-like receptor signaling, cell cycle, AMPK, p53 and NF-kappa B signaling pathways. Taken together, our results suggest that increased FOXM1 expression is associated with poor patient survival and leads to induction of oncomiR miR-186-5p expression and tumor-suppressor inhibition miR-200b-5p, suggesting that the FOXM1/miRNA signaling pathway may contribute to poor patient prognosis and may be a potential therapeutic target in TNBC.
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http://dx.doi.org/10.1016/j.cellsig.2021.109979DOI Listing
March 2021

Variants in TNF and NOS3 (eNOS) genes associated with sepsis in adult patients.

J Gene Med 2021 Apr 26;23(4):e3323. Epub 2021 Feb 26.

Department of Medical Pharmacology, Faculty of Medicine, Gaziantep University, Gaziantep, Turkey.

Background: Sepsis is a life-threatening condition caused by a dysregulated host response to infections and is a leading cause of death in hospitalized patients. The present study aimed to elucidate the possible association between sepsis and the tumor necrosis factor (TNF) gene -308G/A (rs1800629) polymorphism, as well as endothelial nitric oxide synthase (eNOS, NOS3) gene -786T/C (rs2070744), 4a/4b (27 bp-VNTR in intron 4, rs61722009) and 894G/T (Glu298Asp, rs1799983) polymorphisms.

Methods: In total, 188 septic adult cases and 188 healthy controls were enrolled. Genomic DNAs from the controls and patients were analyzed by polymerase chain reaction and restriction fragment length polymorphism methods.

Results: There were significant associations between the G/G genotype and G allele of the TNF -308G/A (rs1800629) polymorphism in the sepsis group (p < 0.001). The presence of the T/C genotype (p = 0.002) and C allele (p = 0.001) of the -786T/C (rs2070744) was markedly associated with an increased risk of sepsis. However, no significant associations were found with 4a/4b (27 bp-VNTR in intron 4, rs61722009) and 894G/T (Glu298Asp, rs1799983) polymorphisms. Higher 4bGC and lower 4bTT haplotype frequencies were associated with sepsis.

Conclusions: Our results strongly suggest that TNF gene (-308G/A, rs1800629) and NOS3 gene -786T/C (rs2070744) polymorphisms may modify individual susceptibility to sepsis in the Turkish population.
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http://dx.doi.org/10.1002/jgm.3323DOI Listing
April 2021

Blood mRNA Expression Profiles of Autophagy, Apoptosis, and Hypoxia Markers on Blood Cardioplegia and Custodiol Cardioplegia Groups.

Braz J Cardiovasc Surg 2021 Jan 1. Epub 2021 Jan 1.

Department of Cardiovascular Surgery, Erciyes University Medical Faculty, Kayseri, Turkey.

Introduction: Blood cardioplegia (BC) and Custodiol cardioplegia (CC) have been used for a long time in open heart surgery and are highly effective solutions. The most controversial issue among these two is whether there is any difference between them regarding myocardial damage after ischemia surgery. In this study, autophagy, apoptosis, and hypoxia markers were investigated and that way we evaluated the differences between BC and CC patients.

Methods: A total of 30 patients were included in this study, using two different cardioplegic solutions. Three different whole blood samples of the patients were taken from a central vein (preoperatively, immediately postoperatively, and one day after surgery). Total ribonucleic acid was extracted from these samples. Quantitative real-time polymerase chain reaction was performed, and changes in gene expression were determined by the 2-ΔΔCt method of relative quantification.

Results: In the CC group, Beclin gene expression level was found to be higher and this difference was statistically significant (P=0.0024). Similarly, cysteine-aspartic acid protease (caspase) 9 and hypoxia-inducible factor 1α messenger ribonucleic acid (mRNA) gene expression level increased and were significantly different in the CC group. In the BC group, Beclin and microtubule-associated protein light chain 3 expressions were higher in the samples taken one day after surgery. Caspases 3 and 8 gene expressions were significantly different in the BC group.

Conclusion: As a result of the analysis performed between the two cardioplegia groups, it has been shown that CC harms the myocardium more than BC at the level of mRNA expression of related markers.
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http://dx.doi.org/10.21470/1678-9741-2020-0330DOI Listing
January 2021

Disregulation of Autophagy in the Transgenerational Cc2d1a Mouse Model of Autism.

Neuromolecular Med 2020 06 13;22(2):239-249. Epub 2019 Nov 13.

Department of Medical Biology, Medical Faculty, Erciyes University, 38039, Kayseri, Turkey.

Autism spectrum disorder (ASD) is a heterogeneously childhood neurodevelopmental disorder, believed to be under development of various genetic and environmental factors. Autophagy and related pathways have also been implicated in the etiology of ASD. We aimed to investigate autophagic markers by generating the transgenerational inheritance of ASD-like behaviors in the Cc2d1a animal model of ASD. Cc2d1a (+/-) mouse model of ASD was built in two different groups by following three generations. After behavior test, bilateral hippocampus was sliced. Western Blot assay and quantitative real-time polymerase chain reaction (QRT-PCR) were used for measurement of LC3 and Beclin-1 as key regulators of autophagy. All of the animal and laboratory studies were conducted in the Erciyes University Genome and Stem Cell Center (GENKOK). Significant LC3 and Beclin-1 mRNA expression levels were observed in mouse hippocampus between groups and generations. Western blot confirmed the changes of the proteins in the hippocampus. LC3 expressions were increased for females and decreased for males compared to the control group. Beclin-1 expression levels were found to be significantly decreased in males and females compared to controls. This study could help explain a new pathway of autophagy in ASD mouse models. Future animal studies need to investigate sex differences in mouse modeling autism-relevant genes like CC2D1A. We anticipate our results to be a starting point for more comprehensive autophagy studies in this mouse model of ASD.
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http://dx.doi.org/10.1007/s12017-019-08579-xDOI Listing
June 2020

Role of circulating microRNAs in acute appendicitis.

Ulus Travma Acil Cerrahi Derg 2018 May;24(3):211-215

Department of Emergency Medicine, Erciyes University Faculty of Medicine, Kayseri-Turkey.

Background: Acute appendicitis (AA) is a momentous, emergency, surgical pathology that has still been investigated for both etiopathogenetic unknowns and challenges in diagnosis. Presently, there is little information about the role of microRNAs (miRNAs), which have basic biological functions in the cell, can be a marker, and are associated with various pathologies, in patients with AA. The aim of this study was to investigate the expressions of some miRNAs in AA.

Methods: Overall, 41 miRNAs were screened in 48 individuals comprising 24 patients with AA and 24 healthy controls at Erciyes University Genome and Stem Cell Center (GENKOK). The obtained data were analyzed using appropriate statistical methods.

Results: miR-29c-3p was found to be increased 2-fold during the first 4-6 h in AA, and this increase was revealed to be statistically significant compared with healthy individuals. Similarly, expressions of let-7b-5p, let-7i-5p, miR-30a-5p, miR-29b-3p, and miR-23a-3p also increased approximately 2-fold in AA, although not statistically significant. No significant differences were found in the screening of the remaining 35 miRNAs in patients with AA.

Conclusion: Although there is little information about the relationship between AA and miRNAs currently, miR-29c-3p was reported to increase in the acute period of AA in this study. With the current results, it can be argued that miR-29c-3p bears the potential to be a marker in patients with AA. The present study may also be a basic research for more extensive and necessary miRNAs screening in this field.
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http://dx.doi.org/10.5505/tjtes.2017.22379DOI Listing
May 2018