CD55 (CD55 Molecule)

Our findings indicate that GDPD5 facilitates EGFR nuclear translocation by binding to CD55, suppressing p53, and causing lipid accumulation and radiotherapy resistance in tumors. Targeting the GDPD5-CD55-EGFR interaction may enhance radiosensitivity.

Therefore, restoring immune recognition and inhibition of proliferation. Hence, thymoquinone could be a potent target for breast cancer therapeutics.

Strategic modulation of complement, whether through genetic, pharmacologic, or antibody-based approaches, could sensitize tumors to immunotherapy and help overcome resistance mechanisms. Continued investigation into this crosstalk will be essential for designing effective combination strategies that maximize antitumor immunity while minimizing immune escape.

Bone metastasis is an adverse prognostic factor for progression-free survival in lung adenocarcinoma patients treated with third-generation EGFR-TKIs. Bone metastasis lesions exhibit a distinct immunosuppressive tumor microenvironment in EGFR-mutant advanced lung adenocarcinoma, in which upregulation of immune regulatory genes in cancer cells and dysfunction of immune cells may constitute a potential mechanism underlying resistance to third-generation EGFR-TKIs.

P4, N=5, Recruiting, Regeneron Pharmaceuticals | Trial completion date: Aug 2029 --> Jan 2030 | Trial primary completion date: Aug 2029 --> Jan 2030

Multivariate ROC curves revealed a diagnostic signature (MM panel) with a sensitivity 86.4% and specificity 91.6%, and a predictive signature (Response panel) with a sensitivity 80% and specificity 91.2%. In conclusion we identified two EV signatures that may have potential as a non-invasive liquid biopsy to complement or replace invasive BM sampling for monitoring patient response to DARA.

By circumventing both complement and antibody responses, SJ-650 significantly inhibited tumor growth in two metastasis models, inducing immunogenic cell death and reprogramming the tumor microenvironment. These findings support SJ-650's potential as a robust oncolytic platform with broad translational applicability.

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.