The polyaromatic hydrocarbon β-naphthoflavone alters binding of YY1, Sp1, and Sp3 transcription factors to the Dp71 promoter in hepatic cells

Carolina Becerril-Esquivel, Katia Peñuelas-Urquides, Erik Blancas-Sánchez, Pablo Zapata-Benavides, Beatriz Silva-Ramírez, Arturo Chávez-Reyes, Fabiola Castorena-Torres, Bulmaro Cisneros, Mario Bermúdez De León

Research output: Contribution to journalArticle

Abstract

© 2018 Kashyap. The smallest product of the Duchenne muscular dystrophy gene, dystrophin (Dp)71, is ubiquitously expressed in nonmuscle tissues. We previously showed that Dp71 expression in hepatic cells is modulated in part by stimulating factor 1 (Sp1), stimulating protein 3 (Sp3), and yin yang 1 (YY1) transcription factors, and that the polyaromatic hydrocarbon, β-naphthoflavone (β-NF), downregulates Dp71 expression. The aim of the present study was to determine whether β-NF represses Dp71 expression by altering mRNA stability or its promoter activity. Reverse transcription-quantitative polymerase chain reaction was used to measure half-life mRNA levels in β -NF-treated cells exposed to actinomycin D, an inhibitor of transcription, for 0, 4, 8, 12 and 16 h. Transient transfections with a plasmid carrying the Dp71 basal promoter fused to luciferase reporter gene were carried out in control and β -NF-treated cells. Electrophoretic mobility shift assays (EMSAs) were performed with labeled probes, corresponding to Dp71 promoter sequences, and nuclear extracts of control and β -NF-treated cells. To the best of our knowledge, the results demonstrated for the first time that this negative regulation takes place at the promoter level rather than the mRNA stability level. Interestingly, using EMSAs, β-NF reduced binding of YY1, Sp1, and Sp3 to the Dp71 promoter. It also suggests that β-NF may modulate the expression of other genes regulated by these transcription factors. In conclusion, β-NF represses Dp71 expression in hepatic cells by altering binding of YY1, Sp1, and Sp3 to the Dp71 promoter.
Original languageEnglish
Pages (from-to)6150-6155
Number of pages6
JournalMolecular Medicine Reports
Volume17
Issue number4
DOIs
Publication statusPublished - 1 Apr 2018

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Transcription Factor 3
Yin-Yang
Hydrocarbons
Hepatocytes
Electrophoretic mobility
Genes
Cells
RNA Stability
Electrophoretic Mobility Shift Assay
Transcription
Messenger RNA
Assays
YY1 Transcription Factor
Transcription Factors
Dystrophin
Proteins
Duchenne Muscular Dystrophy
Polymerase chain reaction
Dactinomycin
Luciferases

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Medicine
  • Molecular Biology
  • Genetics
  • Oncology
  • Cancer Research

Cite this

Becerril-Esquivel, Carolina ; Peñuelas-Urquides, Katia ; Blancas-Sánchez, Erik ; Zapata-Benavides, Pablo ; Silva-Ramírez, Beatriz ; Chávez-Reyes, Arturo ; Castorena-Torres, Fabiola ; Cisneros, Bulmaro ; De León, Mario Bermúdez. / The polyaromatic hydrocarbon β-naphthoflavone alters binding of YY1, Sp1, and Sp3 transcription factors to the Dp71 promoter in hepatic cells. In: Molecular Medicine Reports. 2018 ; Vol. 17, No. 4. pp. 6150-6155.
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abstract = "{\circledC} 2018 Kashyap. The smallest product of the Duchenne muscular dystrophy gene, dystrophin (Dp)71, is ubiquitously expressed in nonmuscle tissues. We previously showed that Dp71 expression in hepatic cells is modulated in part by stimulating factor 1 (Sp1), stimulating protein 3 (Sp3), and yin yang 1 (YY1) transcription factors, and that the polyaromatic hydrocarbon, β-naphthoflavone (β-NF), downregulates Dp71 expression. The aim of the present study was to determine whether β-NF represses Dp71 expression by altering mRNA stability or its promoter activity. Reverse transcription-quantitative polymerase chain reaction was used to measure half-life mRNA levels in β -NF-treated cells exposed to actinomycin D, an inhibitor of transcription, for 0, 4, 8, 12 and 16 h. Transient transfections with a plasmid carrying the Dp71 basal promoter fused to luciferase reporter gene were carried out in control and β -NF-treated cells. Electrophoretic mobility shift assays (EMSAs) were performed with labeled probes, corresponding to Dp71 promoter sequences, and nuclear extracts of control and β -NF-treated cells. To the best of our knowledge, the results demonstrated for the first time that this negative regulation takes place at the promoter level rather than the mRNA stability level. Interestingly, using EMSAs, β-NF reduced binding of YY1, Sp1, and Sp3 to the Dp71 promoter. It also suggests that β-NF may modulate the expression of other genes regulated by these transcription factors. In conclusion, β-NF represses Dp71 expression in hepatic cells by altering binding of YY1, Sp1, and Sp3 to the Dp71 promoter.",
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Becerril-Esquivel, C, Peñuelas-Urquides, K, Blancas-Sánchez, E, Zapata-Benavides, P, Silva-Ramírez, B, Chávez-Reyes, A, Castorena-Torres, F, Cisneros, B & De León, MB 2018, 'The polyaromatic hydrocarbon β-naphthoflavone alters binding of YY1, Sp1, and Sp3 transcription factors to the Dp71 promoter in hepatic cells', Molecular Medicine Reports, vol. 17, no. 4, pp. 6150-6155. https://doi.org/10.3892/mmr.2018.8626, https://doi.org/10.3892/mmr.2018.8626

The polyaromatic hydrocarbon β-naphthoflavone alters binding of YY1, Sp1, and Sp3 transcription factors to the Dp71 promoter in hepatic cells. / Becerril-Esquivel, Carolina; Peñuelas-Urquides, Katia; Blancas-Sánchez, Erik; Zapata-Benavides, Pablo; Silva-Ramírez, Beatriz; Chávez-Reyes, Arturo; Castorena-Torres, Fabiola; Cisneros, Bulmaro; De León, Mario Bermúdez.

In: Molecular Medicine Reports, Vol. 17, No. 4, 01.04.2018, p. 6150-6155.

Research output: Contribution to journalArticle

TY - JOUR

T1 - The polyaromatic hydrocarbon β-naphthoflavone alters binding of YY1, Sp1, and Sp3 transcription factors to the Dp71 promoter in hepatic cells

AU - Becerril-Esquivel, Carolina

AU - Peñuelas-Urquides, Katia

AU - Blancas-Sánchez, Erik

AU - Zapata-Benavides, Pablo

AU - Silva-Ramírez, Beatriz

AU - Chávez-Reyes, Arturo

AU - Castorena-Torres, Fabiola

AU - Cisneros, Bulmaro

AU - De León, Mario Bermúdez

PY - 2018/4/1

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N2 - © 2018 Kashyap. The smallest product of the Duchenne muscular dystrophy gene, dystrophin (Dp)71, is ubiquitously expressed in nonmuscle tissues. We previously showed that Dp71 expression in hepatic cells is modulated in part by stimulating factor 1 (Sp1), stimulating protein 3 (Sp3), and yin yang 1 (YY1) transcription factors, and that the polyaromatic hydrocarbon, β-naphthoflavone (β-NF), downregulates Dp71 expression. The aim of the present study was to determine whether β-NF represses Dp71 expression by altering mRNA stability or its promoter activity. Reverse transcription-quantitative polymerase chain reaction was used to measure half-life mRNA levels in β -NF-treated cells exposed to actinomycin D, an inhibitor of transcription, for 0, 4, 8, 12 and 16 h. Transient transfections with a plasmid carrying the Dp71 basal promoter fused to luciferase reporter gene were carried out in control and β -NF-treated cells. Electrophoretic mobility shift assays (EMSAs) were performed with labeled probes, corresponding to Dp71 promoter sequences, and nuclear extracts of control and β -NF-treated cells. To the best of our knowledge, the results demonstrated for the first time that this negative regulation takes place at the promoter level rather than the mRNA stability level. Interestingly, using EMSAs, β-NF reduced binding of YY1, Sp1, and Sp3 to the Dp71 promoter. It also suggests that β-NF may modulate the expression of other genes regulated by these transcription factors. In conclusion, β-NF represses Dp71 expression in hepatic cells by altering binding of YY1, Sp1, and Sp3 to the Dp71 promoter.

AB - © 2018 Kashyap. The smallest product of the Duchenne muscular dystrophy gene, dystrophin (Dp)71, is ubiquitously expressed in nonmuscle tissues. We previously showed that Dp71 expression in hepatic cells is modulated in part by stimulating factor 1 (Sp1), stimulating protein 3 (Sp3), and yin yang 1 (YY1) transcription factors, and that the polyaromatic hydrocarbon, β-naphthoflavone (β-NF), downregulates Dp71 expression. The aim of the present study was to determine whether β-NF represses Dp71 expression by altering mRNA stability or its promoter activity. Reverse transcription-quantitative polymerase chain reaction was used to measure half-life mRNA levels in β -NF-treated cells exposed to actinomycin D, an inhibitor of transcription, for 0, 4, 8, 12 and 16 h. Transient transfections with a plasmid carrying the Dp71 basal promoter fused to luciferase reporter gene were carried out in control and β -NF-treated cells. Electrophoretic mobility shift assays (EMSAs) were performed with labeled probes, corresponding to Dp71 promoter sequences, and nuclear extracts of control and β -NF-treated cells. To the best of our knowledge, the results demonstrated for the first time that this negative regulation takes place at the promoter level rather than the mRNA stability level. Interestingly, using EMSAs, β-NF reduced binding of YY1, Sp1, and Sp3 to the Dp71 promoter. It also suggests that β-NF may modulate the expression of other genes regulated by these transcription factors. In conclusion, β-NF represses Dp71 expression in hepatic cells by altering binding of YY1, Sp1, and Sp3 to the Dp71 promoter.

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