SOCS1 Inhibits IL-6-Induced CD155 Overexpression in Lung Adenocarcinoma DOI Open Access

Mario Marroquin-Muciño,

Jesus J. Benito-Lopez,

Mario Perez-Medina

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(22), P. 12141 - 12141

Published: Nov. 12, 2024

CD155, also known as the poliovirus receptor (PVR), is a crucial molecule in development and progression of cancer, its overexpression favors immune evasion resistance to immunotherapy. However, little about mechanisms that regulate overexpression. Proinflammatory factors produced by various cellular components tumor microenvironment (TME) have been associated with CD155 expression. We analyzed effect interleukin (IL)-6 on expression lung adenocarcinoma. found positive relationship between mRNA protein levels. This correlation was observed bioinformatics analysis biopsies serum from patients Interestingly, adenocarcinoma cell lines expressing suppressor cytokine signaling 1 (SOCS1) did not show increased levels upon IL-6 stimulation, SOCS1 silencing reverted this effect. are critical regulators Further basic clinical studies needed define role these molecules during improve their impact biomarkers targets for predicting efficacy immunotherapies. study deepens understanding intricate regulation checkpoints mediated soluble allows us devise new ways combine conventional treatments most innovative anticancer options.

Language: Английский

The immune checkpoint TIGIT/CD155 promotes the exhaustion of CD8 + T cells in TNBC through glucose metabolic reprogramming mediated by PI3K/AKT/mTOR signaling DOI Creative Commons
Mingyao Huang, Xiaoqin Yu, Qing Wang

et al.

Cell Communication and Signaling, Journal Year: 2024, Volume and Issue: 22(1)

Published: Jan. 12, 2024

Abstract Objective The CD155/TIGIT axis has attracted considerable interest as an emerging immune checkpoint with potential applications in cancer immunotherapy. Our research focused on investigating the role of checkpoints progression triple-negative breast (TNBC). Methods We evaluated CD155 and TIGIT expression TNBC tissues using both immunohistochemistry (IHC) gene profiling. experiments, vivo vitro, provided evidence that inhibiting pathway reinstates ability CD8 + T cells to generate cytokines. To assess impact signaling blockade, we utilized Glucose Assay Kits Lactate measure alterations glucose lactate levels within cells. employed western blotting (WB) investigate glycolytic-related proteins PI3K/AKT/mTOR pathways following inhibition signaling. Results exhibits heightened a negative correlation extent infiltrating Furthermore, patients demonstrate elevated expression. findings indicate interaction between disrupts metabolism by suppressing activation pathway, ultimately leading reduced production cytokines Both vitro experiments have conclusively demonstrated capacity Moreover, administration blocking antibody against not only inhibits tumor growth but also augments functionality lymphocytes. Conclusions strongly suggest represents promising therapeutic target for treating TNBC.

Language: Английский

Citations

14

LBP-CD155 Liposome Nanovaccine Efficiently Resist Colorectal Cancer and Enhance ICB Therapy DOI Creative Commons

Yajuan Yan,

Ting Duan, Xiaonan Xue

et al.

International Journal of Nanomedicine, Journal Year: 2025, Volume and Issue: Volume 20, P. 1047 - 1063

Published: Jan. 1, 2025

Colorectal cancer (CRC) is a highly malignant and aggressive gastrointestinal tumor. Due to its weak immunogenicity limited immune, cell infiltration lead ineffective clinical outcomes. Therefore, improve the current prophylaxis treatment scheme, offering favorable strategy efficient against CRC urgently needed. Here, we developed nanovaccine (LBP-CD155L NVs) loaded with CD155 gene in liposome, which was modified by Lycium barbarum polysaccharides (LBP) through electrostatic interaction. The characterized transmission electron microscopy Zetasizer. It evaluated vitro, where NVs facilitated endocytosis maturation of DCs, vivo, improved efficacy therapy. In addition, further confirmed mechanisms how TLR4 MGL synergistic pathway endow nanovaccines towards dendritic cells (DCs). Finally, safety tumor immunosuppressive microenvironment were tumor-bearing mouse model. We successfully that facilitates DCs via involving MGL, (DCs) promote differentiation, thereby enhancing cytotoxicity CD8+T cells. Consequently, LBP-CD155L can potentiate prophylactic therapeutic administration model, as evidenced decreased myeloid-derived suppressor (MDSCs) Tregs, reprogrammed macrophage phenotypes, promoted polarization from M2-like macrophages M1-like macrophages, increased effector T Prophylactic combination regimens anti-PD-1 demonstrate synergism stimulates T-cell into tumors counteracts immunosuppression, leading remarkable remission immune checkpoint therapy solid tumors. Our work provided may serve promising tool for reversing ICB CRC.

Language: Английский

Citations

0

CD155 promotes the advancement of hepatocellular carcinoma by suppressing the p53-mediated ferroptosis via interacting with CD96 DOI
Zhenhui Lu,

Jingzhe Yu,

Tuoyu Lu

et al.

Journal of Molecular Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 29, 2025

Language: Английский

Citations

0

Bispecific antibody targeting CD155 mediates T-cell immunotherapy against human gynecological malignancies DOI
Li Ma, Juan Ma,

Feng Dingqing

et al.

Investigational New Drugs, Journal Year: 2025, Volume and Issue: unknown

Published: April 15, 2025

Language: Английский

Citations

0

The evolving landscape of oncolytic virus immunotherapy: combinatorial strategies and novel engineering approaches DOI
Mujibullah Sheikh,

Arshiya Saiyyad,

Aimé Aliunui

et al.

Medical Oncology, Journal Year: 2025, Volume and Issue: 42(6)

Published: May 2, 2025

Language: Английский

Citations

0

Prognostic and diagnostic value of PVR gene and protein levels, serum amylase, and urinary IGFBP-7 and TIMP-2 biomarkers in multiple myeloma DOI Creative Commons

Eman M Habib,

Asmaa M. Hasan,

Shamayel Mohammed

et al.

BMC Cancer, Journal Year: 2025, Volume and Issue: 25(1)

Published: May 14, 2025

Language: Английский

Citations

0

CD8+ T-cell exhaustion: Impediment to triple-negative breast cancer (TNBC) immunotherapy DOI

Dandan Feng,

Dongqing Pu,

Juan Ren

et al.

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, Journal Year: 2024, Volume and Issue: unknown, P. 189193 - 189193

Published: Oct. 1, 2024

Language: Английский

Citations

3

CD155 as an emerging target in tumor immunotherapy DOI

Jiang‐Wan Wu,

Ying Liu, Xing‐Jie Dai

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 131, P. 111896 - 111896

Published: March 22, 2024

Language: Английский

Citations

2

SOCS1 Inhibits IL-6-Induced CD155 Overexpression in Lung Adenocarcinoma DOI Open Access

Mario Marroquin-Muciño,

Jesus J. Benito-Lopez,

Mario Perez-Medina

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(22), P. 12141 - 12141

Published: Nov. 12, 2024

CD155, also known as the poliovirus receptor (PVR), is a crucial molecule in development and progression of cancer, its overexpression favors immune evasion resistance to immunotherapy. However, little about mechanisms that regulate overexpression. Proinflammatory factors produced by various cellular components tumor microenvironment (TME) have been associated with CD155 expression. We analyzed effect interleukin (IL)-6 on expression lung adenocarcinoma. found positive relationship between mRNA protein levels. This correlation was observed bioinformatics analysis biopsies serum from patients Interestingly, adenocarcinoma cell lines expressing suppressor cytokine signaling 1 (SOCS1) did not show increased levels upon IL-6 stimulation, SOCS1 silencing reverted this effect. are critical regulators Further basic clinical studies needed define role these molecules during improve their impact biomarkers targets for predicting efficacy immunotherapies. study deepens understanding intricate regulation checkpoints mediated soluble allows us devise new ways combine conventional treatments most innovative anticancer options.

Language: Английский

Citations

0