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World J Diabetes. May 15, 2011; 2(5): 66-74
Published online May 15, 2011. doi: 10.4239/wjd.v2.i5.66
Nkx6.2 synergizes with Cdx-2 in stimulating proglucagon gene expression
Pei-Xiang Wang, Zhi-Wen Yu, Steven Wong, Tian-Ru Jin
Pei-Xiang Wang, Zhi-Wen Yu, Tian-Ru Jin, Department of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou 510080, Guangdong Province, China
Pei-Xiang Wang, Steven Wong, Tian-Ru Jin, Division of Cell and Molecular Biology, Toronto General Research Institute, University Health Network, M5G 1L7, Canada
Tian-Ru Jin, Department of Medicine, University of Toronto, Toronto, M5G 1L7, Canada
Author contributions: Wang PX performed the major experiments in Figure 1-4; Yu ZW performed mRNA extraction from cell lines and rat intestines. Wong S performed the NKX6 plasmid constructs; and Jin TR and Wang PX wrote the manuscript.
Supported by the Grants from the Canadian Institute of Health Research (CIHR, MOP36398) and Canadian Diabetes Association (1198) to Tianru Jin
Correspondence to: Tian-Ru Jin, PhD, Associate Professor, Department of Medicine and Department of Physiology, University of Toronto, Rm. 10-354, Toronto Medical Discovery Tower, the MaRS Building, 101 College St., Toronto, Ontario, Toronto, Ontario, M5G 1L7, Canada. tianru.jin@utoronto.ca
Telephone: +1-416-581-7670 Fax: +1-416-340-3453
Received: December 23, 2010
Revised: April 11, 2011
Accepted: April 18, 2011
Published online: May 15, 2011
Abstract

AIM: To investigate whether the transactivator of the proglucagon gene (Gcg), Cdx-2, synergizes with other transcription factors in stimulating Gcg expression and the trans-differentiation of Gcg-expressing cells.

METHODS: We conducted affinity chromatography to identify proteins that interact with Cdx-2, using GST-tagged Cdx-2 against cell lysates from pancreatic InR1-G9 and intestinal GLUTag cell lines. This was followed by a mass-spectrometry analysis. From a potential Cdx-2 interaction protein identified, we examined its expression in pancreatic and gut endocrine cells, confirmed its interaction with Cdx-2 by GST-pull down and determined its effect in provoking Gcg expression in cell lines that do not express endogenous Gcg.

RESULTS: We identified 18 potential Cdx-2 interacting proteins. One of them is Nkx6.2. This homeodomain (HD) protein is expressed in pancreatic α and intestinal endocrine L cells but not in insulin producing cell lines, including In111. Nkx6.2, but not Nkx6.1, was shown to interact with Cdx-2, detected by GST-pull down. Furthermore, Nkx6.2 was found to synergize with Cdx-2 in provoking Gcg expression when they were ectopically expressed in the In111 cell line. Finally, when Cdx-2 and Nkx6.2 were co-transfected into the undifferentiated rat intestinal IEC-6 cell line, it produced detectable amount of Gcg mRNA.

CONCLUSION: Cdx-2 recruits Nkx6.2 in exerting its effect in stimulating Gcg expression. Our observations further support the notion that multiple HD proteins, including Cdx-2 and Nkx6.2, are involved in the regulation of Gcg expression and the genesis of Gcg-producing cells.

Keywords: Cdx-2; Nkx6.2; Homeodomain; Proglucagon; Affinity chromatograph