CREB is a key negative regulator of carbonic anhydrase IX (CA9) in gastric cancer

Carbonic anhydrase IX(CA9)is a member of the carbonic anhydrase family that catalyzes the reversible hydration of carbon dioxide, and plays a key role in the regulation of pH. Although a large number of studies have shown that CA9 is strongly up-regulated by HIF1-α, little is known about the negativ...

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Veröffentlicht in:	Cellular signalling 2015-07, Vol.27 (7), p.1369-1379
Hauptverfasser:	Wang, Guanqiao, Cheng, Zhenguo, Liu, Funan, Zhang, Hongyan, Li, Jiabin, Li, Feng
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Anisomycin - pharmacology Antigens, Neoplasm - genetics Antigens, Neoplasm - metabolism Carbonic Anhydrase IX Carbonic Anhydrases - genetics Carbonic Anhydrases - metabolism Cell Line, Tumor CREB-Binding Protein - metabolism Down-Regulation Humans Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Mice Mice, Inbred BALB C Mice, Nude p300-CBP Transcription Factors - metabolism p38 Mitogen-Activated Protein Kinases - chemistry p38 Mitogen-Activated Protein Kinases - metabolism Phosphorylation - drug effects Promoter Regions, Genetic Protein Synthesis Inhibitors - pharmacology RNA, Messenger - metabolism Sirtuin 1 - metabolism Stomach Neoplasms - enzymology Stomach Neoplasms - metabolism Stomach Neoplasms - pathology Transcription, Genetic - drug effects Transplantation, Heterologous
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Zusammenfassung:	Carbonic anhydrase IX(CA9)is a member of the carbonic anhydrase family that catalyzes the reversible hydration of carbon dioxide, and plays a key role in the regulation of pH. Although a large number of studies have shown that CA9 is strongly up-regulated by HIF1-α, little is known about the negative regulation mechanism of CA9 in cancer cells. Here we find that CREB is a key negative regulator of CA9 in gastric cancer. Over-expression of CREB can significantly repress the expression of CA9. Treating with anisomycin (ANS), an activator of p38, the phosphorylation and nuclear translocation of CREB are both promoted, while the transcription of CA9 is repressed. Besides, our results firstly identify that CREB can recruit SIRT1 (class III HDACS) by adaptor protein p300, then repress the expression of CA9. These findings may contribute to understand the negative regulation mechanisms of CA9 in gastric cancer.
ISSN:	0898-6568 1873-3913
DOI:	10.1016/j.cellsig.2015.03.019