CD177 (CD177 Molecule)

CD177+ neutrophils drive liver regeneration by promoting endothelial transmigration, ECM degradation and HGF-α release. These findings reveal a neutrophil-mediated mechanism driving surgical liver regeneration and support the potential of CD177+ neutrophil infusion to establish a proregenerative hepatic environment for therapeutic strategies in liver failure.

Notably, the model retained high accuracy in early-stage CRC (Stage I-II: AUC 0.929, 95% CI 0.868-0.989). Overall, this study provides a robust analytic framework for reproducible whole-blood RNA biomarker discovery and establishes a multi-gene signature with promising translational potential for minimally invasive and early CRC detection.

Our findings suggest that CU06-1004 inhibits inflammation-induced tumorigenesis by modulating the inflammatory response in the colon. Consequently, CU06-1004 could represent a promising therapeutic candidate for the prevention of colorectal cancer through modulation of inflammation.

Additionally, activated CD8+ T cells recruit and activate neutrophils, forming a positive feedback loop. Combining trilaciclib with anti-PD-1 antibodies presents a promising strategy for NSCLC treatment.

In light of these findings, we present a comprehensive review of recent literature concerning the role of CD177 in tumors, inflammatory processes, and autoimmune diseases, with a particular focus on its mediating effects on neutrophil recruitment, transepithelial migration, and the activation of CD177-positive neutrophils, along with the functional implications of CD177 expression beyond neutrophils. A deeper understanding of CD177 may pave the way for the development of novel therapeutic strategies and the assessment of disease prognosis.

The HLA-DRlowCCR2low classical monocyte and CD177+ myelocytes exhibit significant correlations with internal environment and coagulation markers. In septic patients, particularly those patients with cancer, attenuated phagocytic activity of immature neutrophil (myelocytes, metamyelocytes, band neutrophils) and monocyte, and HLA-DRlowCCR2low classical monocyte and CD177+ myelocytes may serve as immunological predictors of poor prognosis.

Genetic or pharmacological inhibition of NET formation decreased necrosis and metastasis, and importantly enhanced chemotherapy efficacy. Altogether, our findings show that NET formation in human CRC is a key feature of tumor necrosis, that it is associated with metastasis, and further suggest that preventing NET formation may offer clinical benefits to CRC patients.

Myeloid-specific deletion of β-galactoside α(2,6)-sialyltransferase 1, which prevented α(2,6)-linked sialic acid incorporation, enhanced GAL1-driven regulatory circuits and accelerated tumor progression, effects that were mitigated by GAL1-neutralizing antibodies. Thus, targeting GAL1-glycan interactions may offer opportunities to reprogram MDSCs and enhance the efficacy of immunotherapeutic and anti-angiogenic strategies.

CD177+ neutrophils play a crucial role in regulating the BMP signaling pathway in IBD, sepsis, and intestinal tumors. These findings offer potential therapeutic targets, but further clinical validation is required to translate them into effective treatment strategies.

• SMARCC1 is highly expressed in lung cancer and promotes the transcription of FLOT1. • FLOT1 overexpression rescues the inhibitory effect of SMARCC1 knockdown on M2 macrophage infiltration and activation of Ferroptosis.

Furthermore, using a CD177 Treg conditional knockout mouse model, we demonstrated that inhibiting CD177 in Tregs significantly impaired their immunosuppressive function and inhibited the progression of hepatocellular carcinoma (HCC) in vitro. Our results underscore the critical role of CD177+ TiTregs in cancer immunology and highlight their potential as novel therapeutic targets in HCC.

The CAFs risk model accurately predicted prognosis, immune cell infiltration, and stromal estimates. The prognostic CAFs (CD177 and CCDC78) may be potential therapeutic targets for CRC.