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761 results on '"Yao, Xiang"'

8. CBX3 antagonizes IFNγ/STAT1/PD-L1 axis to modulate colon inflammation and CRC chemosensitivity

Author

Yao Xiang, Jorge Mata-Garrido, Yuanji Fu, Christophe Desterke, Eric Batsché, Ahmed Hamaï, Christine Sedlik, Youssouf Sereme, David Skurnik, Abdelali Jalil, Rachel Onifarasoaniaina, Eric Frapy, Jean-Christophe Beche, Razack Alao, Eliane Piaggio, Laurence Arbibe, and Yunhua Chang

Subjects
CBX3 (HP1γ), IFNγ Signaling, Colon, Inflammatory/Immune Response, Colorectal Cancer, Medicine (General), R5-920, Genetics, QH426-470
Abstract

Abstract As an important immune stimulator and modulator, IFNγ is crucial for gut homeostasis and its dysregulation links to diverse colon pathologies, such as colitis and colorectal cancer (CRC). Here, we demonstrated that the epigenetic regulator, CBX3 (also known as HP1γ) antagonizes IFNγ signaling in the colon epithelium by transcriptionally repressing two critical IFNγ-responsive genes: STAT1 and CD274 (encoding Programmed death-ligand 1, PD-L1). Accordingly, CBX3 deletion resulted in chronic mouse colon inflammation, accompanied by upregulated STAT1 and CD274 expressions. Chromatin immunoprecipitation indicated that CBX3 tethers to STAT1 and CD274 promoters to inhibit their expression. Reversely, IFNγ significantly reduces CBX3 binding to these promoters and primes gene expression. This antagonist effect between CBX3 and IFNγ on STAT1/PD-L1 expression was also observed in CRC. Strikingly, CBX3 deletion heightened CRC cells sensitivity to IFNγ, which ultimately enhanced their chemosensitivity under IFNγ stimulation in vitro with CRC cells and in vivo with a syngeneic mouse tumor model. Overall, this work reveals that by negatively tuning IFNγ-stimulated immune genes’ transcription, CBX3 participates in modulating colon inflammatory response and CRC chemo-resistance.

Published
2024
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10. LAMA5: A new pathogenic gene for non-syndromic cleft lip with or without cleft palate

Author

Zhenzhen Fu, Yan Qi, Ling-fa Xue, Yao-xiang Xu, Jin Yue, Jin-ze Zhao, Cong Li, and Wenlin Xiao

Subjects
CL/P, LAMA5, Proliferation, Apoptosis, EMT, Shh signal pathway, Medicine (General), R5-920, Biology (General), QH301-705.5
Abstract

Background: This study aimed to investigate the effect of LAMA5 on palatal development in mice. Methods: The palatine process of C57BL/6 J fetal mice on the embryonic day 13.5 (E13.5) was cultured in vitro via the rotating culture method. The LAMA5-shRNA adenovirus vector was constructed, then transfected into the palatal process of E13.5 for 48 h in vitro. A fluorescence microscope was used to visualize the fusion of palates. The expression of LAMA5 was also detected. The expression of ki67, cyclin D1, caspase 3, E-cadherin, vimentin and SHH signaling pathway-related signaling factors in the blank control group, the negative control group, and the LAMA5 interference group were detected after virus transfection. Results: The bilateral palates in the LAMA5 interference group were not fused after virus transfection. PCR and WB showed that the mRNA and protein expressions of LAMA5 were decreased in the LAMA5 interference group. Furthermore, the mRNA and protein expressions of ki67, cyclin D1 and gli1 were decreased in the LAMA5 interference group, while the mRNA and protein expressions of caspase 3 were increased. However, the mRNA and protein expression of E-cadherin, vimentin, Shh and ptch1 did not significantly change in the LAMA5 interference group. Conclusions: LAMA5 silencing causes cleft palate by inhibiting the proliferation of mouse palatal cells and promoting apoptosis, which may not be involved in EMT. LAMA5 silencing can also cause cleft palate by interfering with the SHH signaling pathway.

Published
2024
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