PLAUR (Plasminogen Activator, Urokinase Receptor)

Our findings suggest that there are common molecular profiles between IR and EC. IR-related prognostic model represents an excellent prognosis predictor and immune-related biomarker, which can be applied to risk stratification and precise treatment of EC patients with IR.

Rescue experiments confirmed that PLAUR promotes malignant progression in colorectal cancer via the AKT/p53 pathway. In summary, these findings highlight the potential of PLAUR as a prospective prognostic indicator and a therapeutic target in CRC.

In human PDAC samples, patients with high LDHA expression exhibited greater numbers of M-MDSCs and a higher proportion of uPAR-positive M-MDSCs compared to those with low LDHA expression. These findings provide mechanistic insights into how lactate metabolism in the high-LDHA TME modulates MDSC behavior and contributes to immunosuppression in PDAC.

High PLAUR expression is associated with increased basal cell-like gene expression signatures, copy number instability, and EMT signatures. Mutated TP53-induced PLAUR expression represents a major pathway by which PDAC treatment may lead to chemotherapy resistance and increased cancer cell aggressiveness.

We identified a novel macrophage-related gene signature with clinical utility in HCC. PLAUR promotes immunosuppressive polarization and tumor progression via the PI3K/AKT/mTOR pathway, representing a potential therapeutic target and biomarker for immunotherapy response.

Plasminogen activator urokinase receptor was differently expressed and positively correlated with an unfavorable prognosis in NSCLC. The MIRLET7BHG/hsa-miR-127-3p axis was identified as the most likely upstream ncRNA-related pathway for PLAUR in NSCLC. This study provides insights into the molecular mechanism of action of PLAUR in NSCLC, which may help to develop new drugs to regulate PLAUR expression or its function in tumor development and provide new targets for the treatment of NSCLC.

Accordingly, the overexpression of specific inhibitors targeting these let-7 miRNAs efficiently increases uPAR expression in KG1 cells. These results indicate that selected let-7 miRNAs regulate uPAR expression and impair the adhesion and migration of AML cells.

We also showed that anti-uPAR/PLAUR alone or in combination with anti-programmed cell death protein 1 therapy remarkably curbed tumor growth, using in vitro ICC cell lines and in vivo humanized ICC patient-derived xenograft mouse models. This proof-of-concept study sheds light on the spatially-resolved radiotranscriptomic signature to improve patient selection for emerging immunochemotherapy and high-order immunotherapy combinations in ICC.

CD87×CD3 BiTE and CD87 CAR/IL-12 T-cells showed antigenic specificity and exerted satisfactory cytotoxic effects, decreasing tumor cell proliferation in vitro and reducing existing tumors in experimental mice. Overall, the above findings suggest that CD87 is a promising target for the immunotherapeutic management of iNFPAs using anti-CD87 BiTE and CD87-specific CAR/IL-12 T cells.

PLAUR knockdown notably inhibited ccRCC cell proliferation and migration. Our data suggested that CRRS may be employed as a reliable predictive biomarker that can provide therapeutic benefits for immunotherapy and targeted therapy in ccRCC.

PLAUR may represent a key mechanism underlying ccRCC progression. The involvement of PLAUR in ccRCC progression may be achieved through the activation of the PI3K/AKT/mTOR signaling pathway, making it a reliable biomarker for the identification and prediction of ccRCC.

P4, N=92, Recruiting, Yonsei University | Not yet recruiting --> Recruiting