STAT5 and TET2 Cooperate to Regulate FOXP3-TSDR Demethylation in CD4+ T Cells of Patients with Colorectal Cancer.

Journal of Immunology Research
Hulin MaWeixing Wang

Abstract

The tumor-infiltrating Tregs are linked to colorectal cancer progression and outcome. FOXP3 is regarded as a critical developmental and functional factor for Tregs. FOXP3-TSDR demethylation is required for stable expression of FOXP3 and maintenance of Treg function. In our study, we found specific DNA hypomethylation of FOXP3-TSDR in CD4+ T cells from colon tumor tissues as compared with normal colonic tissues. Moreover, we also found that the expression of STAT5 and TET2 was increased in CD4+ T cells from colon tumor tissues, and the superfluous STAT5 and TET2 binding to FOXP3-TSDR resulted in DNA hypomethylation. In conclusion, we have demonstrated that excessive amounts of STAT5 may bind more TET2 to the FOXP3-TSDR and upregulate FOXP3 expression via DNA demethylation. Our study improved the mechanism of FOXP3-TSDR hypomethylation in tumor-infiltrating CD4+ T cells of CRC patients.

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Citations

Mar 14, 2019·Immunology·Mariela A Moreno AyalaMichel DuPage
Jan 12, 2021·Clinical & Translational Immunology·Juewan KimPatrick Toby Coates
Jun 29, 2021·Frontiers in Immunology·Yujing ZhangRong Jia
Jul 31, 2021·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Yaoyao ChangHaitao Xiao

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Methods Mentioned

BETA
PCR
protein assay
electrophoresis
Immunoprecipitation
transfection

Software Mentioned

Quantity One

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