Williams Cancer Institute

CD276 in Esophageal Squamous Cell Carcinoma (ESCC)

Esophageal squamous cell carcinoma (ESCC) poses a significant challenge in cancer treatment, with immune escape mechanisms contributing to its aggressiveness. Among the pivotal immune checkpoints, CD276 (B7-H3) has emerged as a key player in facilitating tumorigenicity, invasiveness, and metastasis in various cancers. However, its specific role in ESCC immune evasion has remained elusive.

In this study, researchers investigated the expression of CD276 in ESCC tissues from patients using immunohistochemistry (IHC) assays. The results revealed a significant upregulation of CD276 in ESCC tissues, correlating with poor prognosis. This finding underscores the potential importance of CD276 as a therapeutic target in ESCC.

To further elucidate the functional role of CD276 in ESCC, researchers established a 4-nitroquinoline 1-oxide (4NQO)-induced CD276 knockout (CD276wKO) and K14cre; CD276 conditional knockout (CD276cKO) mouse model of ESCC. The findings from in vivo experiments demonstrated that depletion of CD276 inhibited tumorigenesis and progression of ESCC. This highlights CD276 as a potential target for therapeutic intervention in ESCC treatment.

The study also delved into the mechanisms underlying CD276-mediated immune escape in ESCC. Conditional knockout of CD276 in epithelial cells resulted in a significant downregulation of CXCL1, leading to reduced formation of neutrophil extracellular trap networks (NETs) via the CXCL1–CXCR2 signaling axis. Additionally, CD276 depletion augmented natural killer (NK) cells, further enhancing immune surveillance against ESCC.

These findings shed light on the intricate interplay between CD276 and immune surveillance mechanisms in ESCC. Targeting CD276 presents a promising therapeutic approach for ESCC treatment, as it modulates immune responses and inhibits tumorigenesis. By unraveling the role of CD276 in ESCC, this study paves the way for the development of novel therapeutic strategies aimed at bolstering immune surveillance and improving patient outcomes.

In conclusion, this study provides valuable insights into the functional role of CD276 in ESCC and its implications for immune evasion. The findings underscore the potential of targeting CD276 as a therapeutic strategy to enhance immune surveillance and combat ESCC progression. Moving forward, further research and clinical trials are warranted to validate CD276 as a viable therapeutic target in ESCC treatment.

Reference: Gan Xiong, Zhi Chen, Qianwen Liu, Fang Peng, Caihua Zhang, Maosheng Cheng, Rongsong Ling, Shuang Chen, Yu Liang, Demeng Chen, Qimin Zhou. (May 9, 2024). CD276 regulates the immune escape of esophageal squamous cell carcinoma through CXCL1–CXCR2 induced NETs. https://jitc.bmj.com/content/12/5/e008662

Related Posts

Blog 11 de junio de 2024
blog hoy 7 de junio
blog 04 de junio de 2024
1 2 3 113