Class Ⅰ histone deacetylase inhibitor regulate of Mycobacteria–Driven guanylate-binding protein 1 gene expression

Wei, Meili; Qin, Yuexuan; Qian, Kaiqiang; Shang, Shengwen; Zhao, Youqun; Xie, Ting; Xi, Jun; Tang, Bo

doi:10.1016/j.micpath.2022.105655

Microbial Pathogenesis

2022

DOI: 10.1016/j.micpath.2022.105655

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Class Ⅰ histone deacetylase inhibitor regulate of Mycobacteria–Driven guanylate-binding protein 1 gene expression

Meili Wei

Yuexuan Qin²,

Kaiqiang Qian³

et al.

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2024

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Cited by 2 publications

References 39 publications

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DNA hypo-methylation and expression of GBP4 induces T cell exhaustion in pancreatic cancer

Tasiheng,

Lin,

Wang

et al. 2024

Cancer Immunol Immunother

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Immunotherapy for pancreatic ductal carcinoma (PDAC) remains disappointing due to the repressive tumor microenvironment and T cell exhaustion, in which the roles of interferon-stimulated genes were largely unknown. Here, we focused on a typical interferon-stimulated gene, GBP4, and investigated its potential diagnostic and therapeutic value in pancreatic cancer. Expression analysis on both local samples and public databases indicated that GBP4 was one of the most dominant GBP family members present in the PDAC microenvironment, and the expression level of GBP4 was negatively associated with patient survival. We then identified DNA hypo-methylation in regulatory regions of GBP4 in PDAC, and validated its regulatory role on GBP4 expression via performing targeted methylation using dCas9-SunTag-DNMAT3A-sgRNA-targeted methylation system on selected DNA locus. After that, we investigated the downstream functions of GBP4, and chemotaxis assays indicated that GBP4 overexpression significantly improved the infiltration of CD8 + T cells, but also induced upregulation of immune checkpoint genes and T cell exhaustion. Lastly, in vitro T cell killing assays using primary organoids suggested that the PDAC samples with high level of GBP4 expression displayed significantly higher sensitivity to anti-PD-1 treatment. Taken together, our studies revealed the expression patterns and epigenetic regulatory mechanisms of GBP4 in pancreatic cancer and clarified the effects of GBP4 on T cell exhaustion and antitumor immunology. Supplementary Information The online version contains supplementary material available at 10.1007/s00262-024-03786-3.

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DNA hypo-methylation and expression of GBP4 induces T cell exhaustion in pancreatic cancer

Tasiheng,

Lin,

Wang

et al. 2024

Cancer Immunol Immunother

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Inhibition of GBP1 alleviates pyroptosis of human pulmonary microvascular endothelial cells through STAT1/NLRP3/GSDMD pathway

Hao,

Fu,

et al. 2024

Molecular Immunology

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Class Ⅰ histone deacetylase inhibitor regulate of Mycobacteria–Driven guanylate-binding protein 1 gene expression

Cited by 2 publications

References 39 publications

DNA hypo-methylation and expression of GBP4 induces T cell exhaustion in pancreatic cancer

DNA hypo-methylation and expression of GBP4 induces T cell exhaustion in pancreatic cancer

Inhibition of GBP1 alleviates pyroptosis of human pulmonary microvascular endothelial cells through STAT1/NLRP3/GSDMD pathway

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