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Sal-like protein 2 upregulates p16 expression through a proximal promoter element.

Wu Z, Cheng K, Shi L, Li Z, Negi H, Gao G, Kamle S, Li D - Cancer Sci. (2015)

Bottom Line: Promoter-reporter assays of p16(INK4A) and several other tumor-related genes indicated that the Sall2 regulation of these promoters was not significantly different between the two major forms of Sall2 with alternative exon 1 or exon 1A.Finally, to confirm the significance of Sall2-activated p16 expression in cell cycle regulation, we co-transfected the SKOV3 cells with a Sall2 expression construct and a p16 minigene and also co-transfected the ES-2 cells with a Sall2 expression construct and the siRNA against p16 for flow cytometry analysis.Our results showed that Sall2 enhanced the p16 minigene blocking of cell cycle progression and p16 knockdown with siRNA abolished most of the Sall2 inhibition of cell cycle progression.

View Article: PubMed Central - PubMed

Affiliation: School of Pharmacy, Shanghai Jiao Tong University, Shanghai, China.

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Comparative genomic analysis of p16 promoter region. Schematic diagram shows comparative genomic analysis of p16 promoter regions using ECR browser program (http://ecrbrowser.dcode.org). The DNA sequence of humans is compared with corresponding sequences of mice, dogs and monkeys. Areas with >50% sequence similarities are depicted above the black line.
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fig06: Comparative genomic analysis of p16 promoter region. Schematic diagram shows comparative genomic analysis of p16 promoter regions using ECR browser program (http://ecrbrowser.dcode.org). The DNA sequence of humans is compared with corresponding sequences of mice, dogs and monkeys. Areas with >50% sequence similarities are depicted above the black line.

Mentions: We also analyzed the p16 promoter for conserved regions using Dcode ECR Brower (Fig.6).25 Surprisingly, the DNA sequence of the human p16 promoter region had little homology with other mammals, other than dogs and monkeys around the two potential ID1-associated HLH transcription factor binding sites. In the deletion analysis, only the second ID1-associated HLH transcription factor binding site is required for high-level p16 promoter activity (Fig.4a).


Sal-like protein 2 upregulates p16 expression through a proximal promoter element.

Wu Z, Cheng K, Shi L, Li Z, Negi H, Gao G, Kamle S, Li D - Cancer Sci. (2015)

Comparative genomic analysis of p16 promoter region. Schematic diagram shows comparative genomic analysis of p16 promoter regions using ECR browser program (http://ecrbrowser.dcode.org). The DNA sequence of humans is compared with corresponding sequences of mice, dogs and monkeys. Areas with >50% sequence similarities are depicted above the black line.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4376433&req=5

fig06: Comparative genomic analysis of p16 promoter region. Schematic diagram shows comparative genomic analysis of p16 promoter regions using ECR browser program (http://ecrbrowser.dcode.org). The DNA sequence of humans is compared with corresponding sequences of mice, dogs and monkeys. Areas with >50% sequence similarities are depicted above the black line.
Mentions: We also analyzed the p16 promoter for conserved regions using Dcode ECR Brower (Fig.6).25 Surprisingly, the DNA sequence of the human p16 promoter region had little homology with other mammals, other than dogs and monkeys around the two potential ID1-associated HLH transcription factor binding sites. In the deletion analysis, only the second ID1-associated HLH transcription factor binding site is required for high-level p16 promoter activity (Fig.4a).

Bottom Line: Promoter-reporter assays of p16(INK4A) and several other tumor-related genes indicated that the Sall2 regulation of these promoters was not significantly different between the two major forms of Sall2 with alternative exon 1 or exon 1A.Finally, to confirm the significance of Sall2-activated p16 expression in cell cycle regulation, we co-transfected the SKOV3 cells with a Sall2 expression construct and a p16 minigene and also co-transfected the ES-2 cells with a Sall2 expression construct and the siRNA against p16 for flow cytometry analysis.Our results showed that Sall2 enhanced the p16 minigene blocking of cell cycle progression and p16 knockdown with siRNA abolished most of the Sall2 inhibition of cell cycle progression.

View Article: PubMed Central - PubMed

Affiliation: School of Pharmacy, Shanghai Jiao Tong University, Shanghai, China.

Show MeSH
Related in: MedlinePlus