Matrix gla protein mediates CD8+ T-cell exhaustion to facilitate immune evasion in intrahepatic cholangiocarcinoma DOI Open Access
Xiaohan Cao, Stephan Lang, Yulei Xie

et al.

CytoJournal, Journal Year: 2025, Volume and Issue: 22, P. 41 - 41

Published: April 1, 2025

Objective Matrix Gla protein (MGP) has been found to be strongly associated with cancer progression. However, its role in intrahepatic cholangiocarcinoma (ICC) remains unclear, particularly within the tumor immune microenvironment. MGP may promote evasion by activating nuclear factor-kappa-light-chain-enha ncer of activated B-cells (NF-κB) signaling pathway, which increases expression programmed death-ligand 1 (PD-L1) and contributes CD8 + T-cell exhaustion. This research mainly aims examine regulatory ICC. Material Methods ICC xenograft mouse models human cell line (HuCCT1) were established evaluate patterns. knockdown or overexpression HuCCT1 cells was co-incubated antigen-specific T cells, flow cytometry used detect markers The effects modulation on PD-L1 assessed immunohistochemistry immunofluorescence. Western blotting employed analyze impact NF-κB signaling. In addition, p65 co-transfected study their combined exhaustion markers. Cell proliferation apoptosis evaluated through colony formation assays cytometry. Results Compared adjacent tissues cholangiocellular epithelial significantly overexpressed ( P < 0.001). led phosphorylation 0.001), elevated heightened levels Conversely, mitigated 0.01) 0.01 while also reducing 0.01). Conclusions promotes facilitates pathway activation.

Language: Английский

Matrix gla protein mediates CD8+ T-cell exhaustion to facilitate immune evasion in intrahepatic cholangiocarcinoma DOI Open Access
Xiaohan Cao, Stephan Lang, Yulei Xie

et al.

CytoJournal, Journal Year: 2025, Volume and Issue: 22, P. 41 - 41

Published: April 1, 2025

Objective Matrix Gla protein (MGP) has been found to be strongly associated with cancer progression. However, its role in intrahepatic cholangiocarcinoma (ICC) remains unclear, particularly within the tumor immune microenvironment. MGP may promote evasion by activating nuclear factor-kappa-light-chain-enha ncer of activated B-cells (NF-κB) signaling pathway, which increases expression programmed death-ligand 1 (PD-L1) and contributes CD8 + T-cell exhaustion. This research mainly aims examine regulatory ICC. Material Methods ICC xenograft mouse models human cell line (HuCCT1) were established evaluate patterns. knockdown or overexpression HuCCT1 cells was co-incubated antigen-specific T cells, flow cytometry used detect markers The effects modulation on PD-L1 assessed immunohistochemistry immunofluorescence. Western blotting employed analyze impact NF-κB signaling. In addition, p65 co-transfected study their combined exhaustion markers. Cell proliferation apoptosis evaluated through colony formation assays cytometry. Results Compared adjacent tissues cholangiocellular epithelial significantly overexpressed ( P < 0.001). led phosphorylation 0.001), elevated heightened levels Conversely, mitigated 0.01) 0.01 while also reducing 0.01). Conclusions promotes facilitates pathway activation.

Language: Английский

Citations

0