CD147‐K148me2‐Driven Tumor Cell‐Macrophage Crosstalk Provokes NSCLC Immunosuppression via the CCL5/CCR5 Axis DOI Creative Commons
Ke Wang, Xiaohong Chen, Lin Peng

и другие.

Advanced Science, Год журнала: 2024, Номер 11(29)

Опубликована: Июнь 14, 2024

Abstract Immunosuppression is a major hallmark of tumor progression in non‐small cell lung cancer (NSCLC). Cluster differentiation 147 (CD147), an important pro‐tumorigenic factor, closely linked to NSCLC immunosuppression. However, the role CD147 di‐methylation immunosuppressive microenvironment (TME) remains unclear. Here, at Lys148 (CD147‐K148me2) identified as common post‐translational modification (PTM) that significantly associated with unsatisfying survival outcomes among sufferers, especially those advanced stages disease. The methyltransferase NSD2 catalyzes generate CD147‐K148me2. Further analysis demonstrates CD147‐K148me2 reestablishes TME and promotes progression. Mechanistically, this interaction between cyclophilin A (CyPA) CD147, turn, increases CCL5 gene transcription by activating p38‐ZBTB32 signaling, leading increased cell‐derived secretion. Subsequently, CD147‐K148me2‐mediated upregulation facilitates M2‐like tumor‐associated macrophage (TAM) infiltration tissues via CCL5/CCR5 axis‐dependent intercellular crosstalk cells macrophages, which inhibited blocking targeted antibody 12C8. Overall, study reveals CD147‐K148me2‐driven development immunosuppression, provides potential interventional strategy for PTM‐targeted therapy.

Язык: Английский

CD8+ T cell exhaustion and its regulatory mechanisms in the tumor microenvironment: key to the success of immunotherapy DOI Creative Commons
Biao Zhang,

Jinming Liu,

Yuying Mo

и другие.

Frontiers in Immunology, Год журнала: 2024, Номер 15

Опубликована: Сен. 20, 2024

A steady dysfunctional state caused by chronic antigen stimulation in the tumor microenvironment (TME) is known as CD8 + T cell exhaustion. Exhausted-like cells (CD8 Tex) displayed decreased effector and proliferative capabilities, elevated co-inhibitory receptor generation, cytotoxicity, changes metabolism transcription. TME induces exhaustion through long-term stimulation, upregulation of immune checkpoints, recruitment immunosuppressive cells, secretion cytokines. Tex may be both reflection cancer progression reason for poor control. The successful outcome current immunotherapies, which include checkpoint blockade adoptive treatment, depends on Tex. In this review, we are interested intercellular signaling network interacting with These findings provide a unique detailed perspective, helpful changing completely unpopular hypofunction intensifying effect immunotherapy.

Язык: Английский

Процитировано

4
A silence catalyst: CCL5-mediated intercellular communication in cancer DOI

Wei‐Ting Hu,

Min Li, Peijun Ma

и другие.

Archives of Toxicology, Год журнала: 2025, Номер unknown

Опубликована: Апрель 1, 2025

Язык: Английский

Процитировано

0
CD147‐K148me2‐Driven Tumor Cell‐Macrophage Crosstalk Provokes NSCLC Immunosuppression via the CCL5/CCR5 Axis DOI Creative Commons
Ke Wang, Xiaohong Chen, Lin Peng

и другие.

Advanced Science, Год журнала: 2024, Номер 11(29)

Опубликована: Июнь 14, 2024

Abstract Immunosuppression is a major hallmark of tumor progression in non‐small cell lung cancer (NSCLC). Cluster differentiation 147 (CD147), an important pro‐tumorigenic factor, closely linked to NSCLC immunosuppression. However, the role CD147 di‐methylation immunosuppressive microenvironment (TME) remains unclear. Here, at Lys148 (CD147‐K148me2) identified as common post‐translational modification (PTM) that significantly associated with unsatisfying survival outcomes among sufferers, especially those advanced stages disease. The methyltransferase NSD2 catalyzes generate CD147‐K148me2. Further analysis demonstrates CD147‐K148me2 reestablishes TME and promotes progression. Mechanistically, this interaction between cyclophilin A (CyPA) CD147, turn, increases CCL5 gene transcription by activating p38‐ZBTB32 signaling, leading increased cell‐derived secretion. Subsequently, CD147‐K148me2‐mediated upregulation facilitates M2‐like tumor‐associated macrophage (TAM) infiltration tissues via CCL5/CCR5 axis‐dependent intercellular crosstalk cells macrophages, which inhibited blocking targeted antibody 12C8. Overall, study reveals CD147‐K148me2‐driven development immunosuppression, provides potential interventional strategy for PTM‐targeted therapy.

Язык: Английский

Процитировано

3