Publications by authors named "Bartosz Adam Frycz"

5 Publications

  • Page 1 of 1

mRNA expression of steroidogenic enzymes, steroid hormone receptors and their coregulators in gastric cancer.

Oncol Lett 2017 May 21;13(5):3369-3378. Epub 2017 Mar 21.

Department of Biochemistry and Molecular Biology, Poznań University of Medical Sciences, 60-781 Poznań, Poland.

Epidemiological and experimental findings suggest that the development of gastric cancer (GC) is regulated by steroid hormones. In postmenopausal women and older men, the majority of steroid hormones are produced locally in peripheral tissue through the enzymatic conversion of steroid precursors. Therefore, using reverse transcription-quantitative polymerase chain reaction analysis, the mRNA expression of genes encoding steroidogenic enzymes, including steroid sulfatase (STS), hydroxy-delta-5-steroid dehydrogenase 3 beta- and steroid delta-isomerase 1 (HSD3B1), 17β-hydroxysteroid dehydrogenase type 7 and aromatase (CYP19A1), was investigated in primary tumoral and adjacent healthy gastric mucosa from 60 patients with GC. Furthermore, the mRNA levels for estrogen receptor α, estrogen receptor β (ESR2) and androgen receptor (AR), along with their coregulators, including proline, glutamate and leucine rich protein 1, CREB binding protein, nuclear receptor coactivator 1 (NCOA1), nuclear receptor corepressor 1 (NCOR1) and nuclear receptor subfamily 2 group F member 1 (NR2F1), were investigated. Additionally, the association between the mRNA expression of these genes and the clinicopathological features of patients with GC was examined. Significantly decreased levels of STS, HSD3B1, ESR2, AR, NCOA1 and NCOR1 mRNA, in addition to significantly increased levels of CYP19A1 mRNA were demonstrated in tumoral tissue samples compared with adjacent healthy gastric tissue samples. Deregulated expression of these genes in the analyzed tissue samples was associated with certain clinicopathological features of GC, such as age and localization of the tumor. The results of the current study suggest that all of the genes analyzed are expressed in tumoral and adjacent healthy gastric mucosa. In addition, the results indicate that abnormal expression of STS, ESR2, AR, NCOA1 and NCOR1 may serve a role in the development and progression of GC, and may be associated with specific clinicopathological features in patients with GC.
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http://dx.doi.org/10.3892/ol.2017.5881DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5431337PMC
May 2017

Transcript level of AKR1C3 is down-regulated in gastric cancer.

Biochem Cell Biol 2016 Apr 10;94(2):138-46. Epub 2015 Dec 10.

a Department of Biochemistry and Molecular Biology, University of Medical Sciences, Poznań, Poland.

Steroid hormones have been shown to play a role in gastric carcinogenesis. Large amounts of steroid hormones are locally produced in the peripheral tissues of both genders. Type 5 of 17β-hydroxysteroid dehydrogenase, encoded by the AKR1C3 gene, plays a pivotal role in both androgen and estrogen metabolism, and its expression was found to be deregulated in different cancers. In this study we measured AKR1C3 transcript and protein levels in nontumoral and primary tumoral gastric tissues, and evaluated their association with some clinicopathological features of gastric cancer (GC). We found decreased levels of AKR1C3 transcript (p < 0.0001) and protein (p = 0.0021) in GC tissues compared with the adjacent, apparently histopathologically normal, mucosa. Lower levels of AKR1C3 transcript were observed in diffuse and intestinal types of GC, whereas AKR1C3 protein levels were decreased in tumors with multisite localization, in diffuse histological type, T3, T4, and G3 grades. We also determined the effect of the histone deacetylase inhibitor sodium butyrate (NaBu) on AKR1C3 expression in EPG 85-257 and HGC-27 GC cell lines. We found that NaBu elevates the levels of both AKR1C3 transcript and protein in the cell lines we investigated. Together, our results suggest that decreased expression of AKR1C3 may be involved in development of GC and can be restored by NaBu.
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http://dx.doi.org/10.1139/bcb-2015-0096DOI Listing
April 2016

Expression of 17β-hydroxysteroid dehydrogenase type 2 is associated with some clinicopathological features in gastric cancer.

Biomed Pharmacother 2015 Mar 9;70:24-7. Epub 2015 Jan 9.

Department of Biochemistry and Molecular Biology, Poznań University of Medical Sciences, Poznań, Poland. Electronic address:

In most populations, gastric cancer (GC) incidence is higher in men than in women, which may suggest the role of sex steroid hormones in gastric cancerogenesis. Both, androgens and estrogens can be synthetised in peripherial tissues. This process is controlled by expression of steroidogenic enzymes. Therefore, we evaluate the 17β-hydroxysteroid dehydrogenase type 2 (HSD17B2) transcript and protein levels in gastric tumoral and nontumoral tissue. We also determined the association between HSD17B2 transcript and protein levels and some clinicopathological features in GC. We found significantly decreased levels of HSD17B2 transcript (P=0.00072) and protein (P=0.00017) in primary tumoral tissues of GC patients, as compared to nontumoral tissues. In patients above 60 years of age the amounts of HSD17B2 transcript (P=0.00044) and protein (P=0.00027) were significantly lower in tumoral than nontumoral tissues. Similarly, lower HSD17B2 levels, both in terms of the transcript and protein, were observed in tumoral tissues of male (P=0.013, P=0.0014), patients stomach (P=0.0062, P=0.045) and cardia (P=0.02, P=0.02) site of tumor, T3 (P=0.018, P=0.014) depth of invasion, N0 (P=0.017, P=0.045) lymph node metastasis, G3 (P=0.0027, P=0.014) malignancy grade. We also observed significantly reduced level of HSD17B2 transcript in tumoral tissue specimens of females (P=0.014), T4 depth of invasion (P=0.02), N3 lymph node metastasis (P=0.037) and G2 malignancy grade (P=0.045). Furthermore, diffuse GC histological types were associated with lower HSD17B2 protein level (P=0.024) than nontumoral tissues. We demonstrated that HSD17B2 transcript and protein levels are linked to some clinicopathological features in GC.
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http://dx.doi.org/10.1016/j.biopha.2014.12.042DOI Listing
March 2015

Decreased expression of ten-eleven translocation 1 protein is associated with some clinicopathological features in gastric cancer.

Biomed Pharmacother 2014 Mar 21;68(2):209-12. Epub 2014 Jan 21.

Department of Biochemistry and Molecular Biology, Poznań University of Medical Sciences, Poznań, Poland. Electronic address:

A decrease in ten-eleven translocation 1 (TET1) transcript and 5-Hydroxymethylcytosine (5hmC) levels has recently been demonstrated in primary gastric cancer (GC). However, little is known about TET1 protein levels in gastric tumoral and nontumoral tissue. Therefore, using reverse transcription, real-time quantitative polymerase chain reaction and western blotting analysis, we determined the TET1 transcript and protein levels in tumoral and nontumoral tissue from 38 patients with GC. We also assessed the association between the decrease in TET1 transcript and protein levels and some clinicopathological features in primary GC. We found significantly decreased levels of TET1 transcript (P=0.0023) and protein (P=0.00024) in primary tumoral tissues as compared to nontumoral tissues in patients with GC. Moreover, we also observed significantly lower amounts of TET1 transcript (P=0.03) and protein (P=0.00018) in tumoral tissues in patients aged>60. We also found significant lowered TET1 protein levels in male patients (P=0.0014), stomach (P=0.044) and cardia (P=0.013) tumor localization, T3 depth of invasion (P=0.019), N1 (P=0.012) and N3 lymph node metastasis (P=0.013) and G3 histological grade (P=0.0012). There were also significant decreases in TET1 transcript levels in female patients (P=0.042), intestinal histological types (P=0.0079) and T4 depth of invasion (P=0.037). Our results demonstrated that a decrease in TET1 transcript and protein levels is associated with some clinicopathological features in GC.
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http://dx.doi.org/10.1016/j.biopha.2013.12.011DOI Listing
March 2014

Expression of 17β-hydroxysteroid dehydrogenase type 1 in gastric cancer.

Biomed Pharmacother 2013 Sep 9;67(7):651-7. Epub 2013 Jul 9.

Department of Biochemistry and Molecular Biology, Poznań University of Medical Sciences, 6 Święcickiego St., 60-781 Poznań, Poland. Electronic address:

There are several findings suggesting the protective role of estrogens in gastric carcinogenesis. Extragonadal 17β-estradiol (E2) may be formed during estrone (E1) reduction to E2 by 17-β-hydroxysteroid dehydrogenase type 1 (HSD17B1). Therefore, we studied the HSD17B1 transcript and protein levels in primary nontumoral and tumoral gastric tissue from the same 21 patients with gastric cancer (GC). We also assessed the effect of 5-Aza-2'-deoxycytidine (5-dAzaC), on the methylation status of HSD17B1 and its expression and conversion of E1 to E2 in HGC-27 and EPG 85-257 GC cells. We identified the presence of HSD17B1 transcript and protein in HGC-27 and EPG 85-257 GC cells as well as in primary nontumoral and tumoral tissues from patients with GC. Moreover, we found that 5-dAzaC significantly up-regulated the HSD17B1 transcript and protein levels, which is associated with increased conversion of E1 to E2 in HGC-27 and EPG 85-257 GC cells. The changes in HSD17B1 expression in both HGC-27 and EPG 85-257 cells were accompanied by 5-dAzaC induced DNA demethylation in the 5' flanking region. Our results demonstrated that HSD17B1 expression and its ability to convert the weak estrogen E1 to the more potent E2 can be associated with DNA methylation in the 5' flanking region in GC cells.
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http://dx.doi.org/10.1016/j.biopha.2013.06.012DOI Listing
September 2013
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