Effect of Benzo(a)pyrene on the Expression of miR-483-3p in Hepatocyte Primary Culture and Rat Liver. / Filippov, S. V.; Yarushkin, A. A.; Kalinina, T. S. et al.
In: Biochemistry (Moscow), Vol. 84, No. 10, 01.10.2019, p. 1197-1203.Research output: Contribution to journal › Article › peer-review
}
TY - JOUR
T1 - Effect of Benzo(a)pyrene on the Expression of miR-483-3p in Hepatocyte Primary Culture and Rat Liver
AU - Filippov, S. V.
AU - Yarushkin, A. A.
AU - Kalinina, T. S.
AU - Ovchinnikov, V. Y.
AU - Knyazev, R. A.
AU - Gulyaeva, L. F.
PY - 2019/10/1
Y1 - 2019/10/1
N2 - Here, we suggested that the epigenetic mechanism of benzo(a)pyrene (BP) action might be based on the aryl hydrocarbon receptor (AhR)-mediated transcription of the target genes, including miRNAs, that have the dioxin response element (DRE) in their promoters. The effect of BP on the expression of the oncogenic miR-483-3p, its host gene IGF2, and target gene IGF1 in primary hepatocytes and in the liver of Wistar female rats was investigated. The activation of AhR was confirmed using selective AhR inhibitor CH-223191 and by evaluating expression of the target CYP1A1 gene. The lack of coordination between the expression of miR-483-3p and its host gene IGF2 was revealed, which may be due to the presence of the binding site for the estrogen receptor alpha (ERα), which is a negative expression regulator. Our results confirm the existence of the AhR-mediated pathway in the regulation of expression of miR-483-3p, IGF1, and IGF2 under BP exposure, which is of considerable interest for understanding the epigenetic mechanisms of the carcinogenic effect of BP.
AB - Here, we suggested that the epigenetic mechanism of benzo(a)pyrene (BP) action might be based on the aryl hydrocarbon receptor (AhR)-mediated transcription of the target genes, including miRNAs, that have the dioxin response element (DRE) in their promoters. The effect of BP on the expression of the oncogenic miR-483-3p, its host gene IGF2, and target gene IGF1 in primary hepatocytes and in the liver of Wistar female rats was investigated. The activation of AhR was confirmed using selective AhR inhibitor CH-223191 and by evaluating expression of the target CYP1A1 gene. The lack of coordination between the expression of miR-483-3p and its host gene IGF2 was revealed, which may be due to the presence of the binding site for the estrogen receptor alpha (ERα), which is a negative expression regulator. Our results confirm the existence of the AhR-mediated pathway in the regulation of expression of miR-483-3p, IGF1, and IGF2 under BP exposure, which is of considerable interest for understanding the epigenetic mechanisms of the carcinogenic effect of BP.
KW - AhR
KW - benzo(a)pyrene
KW - DRE
KW - ERα
KW - induction
KW - microRNA
KW - target genes
KW - BREAST-CANCER
KW - ARYL-HYDROCARBON RECEPTOR
KW - ALPHA
KW - IDENTIFICATION
KW - ER alpha
UR - http://www.scopus.com/inward/record.url?scp=85073598641&partnerID=8YFLogxK
U2 - 10.1134/S0006297919100080
DO - 10.1134/S0006297919100080
M3 - Article
C2 - 31694515
AN - SCOPUS:85073598641
VL - 84
SP - 1197
EP - 1203
JO - Biochemistry (Moscow)
JF - Biochemistry (Moscow)
SN - 0006-2979
IS - 10
ER -
ID: 21926812