CD55 (CD55 Molecule)

Through MR analysis, this study systematically identified 10 hub genes associated with AD and predicted 5 potential drug candidates. These findings offer novel insights into the molecular mechanisms underlying AD and may contribute to improved strategies for clinical diagnosis and targeted therapy.

We elucidated the relationship between UC and hypoxia/mitophagy and identified potential diagnostic biomarkers. This study provides a reference for the future development of targeted treatment strategies to improve diagnostic and therapeutic protocols for UC.

Flow cytometric analysis conducted for proteomic expression of CD46 and CD55 on cell surfaces of leukemia patients showed a reduction in expression by 1.2-fold and 2.8-fold in AML patients, respectively. Post transcriptional knockdown of both genes in leukemic cell model using customized shRNA, followed by cell viability assays showed a significant reduction in the viability of cells by 3-fold, suggesting that although the expression of both proteins could be compromised by cancerous cells to evade complement attack mechanisms, they could also be vital to the viability of cancerous cells suggesting a dual role of complement in the tumor microenvironment.

Pre-treatment with EGCG blocked EGF-induced changes in CC cells. Collectively, these findings indicate the inflammatory role for EGF and attest the anti-inflammatory potential of EGCG in CC cells.

The high expression of CD55 was related to poor prognosis of TETs. Moreover, its significant association with worse outcomes in high-risk TETs subgroup further underscores it its potential as a prognostic marker and therapeutic target, especially in TSCC.

EGCG, by targeting TGF-β and modulating PD-L1 and mCRPs, represents a promising candidate for immunotherapeutic development in CC.

A neutralizing antibody to the hADGRE5 ligand CD55 significantly dampened MS-induced β-Arr2 engagement. Overall, this study advances our understanding of hADGRE5's signaling and highlights the receptor's plasticity in activating pathways via both GPS cleavage-dependent and -independent mechanisms.

These findings demonstrate that surface biotinylation improves the sensitivity and selectivity of plasma membrane proteomics under hypoxia, revealing hypoxia-responsive proteins and pathways not captured by standard whole-cell analysis.

This work revealed that several GP-CFs from Decay-accelerating factor (CD55), Versican (VCAN), Carboxypeptidase Z (CPZ)and Mucin 16 (MUC16) have the potential to distinguish PDAC NATs from Ts, with an area under the curve (AUC) of 1 in the validation cohort. These data demonstrate that CF glycoproteins may associated with PDAC development and progression and have potential as candidate biomarkers for clinical decision-making.

Correlative analyses in patient cohorts and therapeutic effects in preclinical models support the clinical relevance of this pathway. Our findings uncover a novel mechanism by which MAFB promotes ovarian cancer progression through cytoskeletal remodeling and immune suppression, connecting transcriptional regulation with epitranscriptomic modifications, and identify the MAFB-WTAP-CD55 axis as a potential therapeutic target in ovarian cancer.

Our findings identify PD-1+ CD8+ T cells and PD-1+ FoxP3+ Tregs as potential biomarkers of resistance to neoadjuvant chemoimmunotherapy in gastric cancer. Transcriptional programs centered on IL1B/CXCL5 and LGALS3/IDO1 define distinct immune phenotypes that may guide future combination strategies targeting both effector and suppressive arms of the tumor immune response.

While complement modulation does not significantly alter RT-induced DNA-damage repair mechanisms or intrinsic radiosensitivity in cancer cells, our results suggest that combining RT with complement-based anti-cancer therapy may enhance complement-dependent cytotoxicity (CDC) and apoptosis in tumor cells. This study sheds light on the complex interplay between RT and the complement system, offering insights into potential novel combinatorial therapeutic strategies and a potential sequential structure for certain tumor types.