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PRDX2 induces tumor immune evasion by modulating the HDAC3-Galectin-9 axis in lung adenocarcinoma cells.
J Transl Med
January 2025
Joint Research Center for Occupational Medicine and Health of IHM, School of Medicine, Anhui University of Science and Technology, Huainan, Anhui, 232000, China.
Background: PRDX2 is significantly expressed in various cancers and is associated with the proliferation of tumor cells. Nonetheless, the precise mechanism of PRDX2 in tumor immunity remains incompletely understood. This study aims to investigate the impact of PRDX2, which is highly expressed in lung adenocarcinoma, on T cells in the tumor immune microenvironment, and its immune action target to promote the immune escape of lung cancer cells, to provide a theoretical basis for lung adenocarcinoma treatment with PRDX2 as the target.
View Article and Find Full Text PDFProtocatechuic aldehyde sensitizes BRAF-mutant melanoma cells to temozolomide through inducing FANCD2 degradation.
Med Oncol
January 2025
Engineering Research Center of Sichuan-Tibet Traditional Medicinal Plant, Chengdu University, Chengdu, 610106, China.
Temozolomide (TMZ)-based chemotherapy is a primary regimen for melanoma patients who have failed targeted therapy or immunotherapy. However, the low response rate of TMZ-based chemotherapy challenges the patients' prognosis. BRAF mutation is the most frequently mutated site in melanoma.
View Article and Find Full Text PDFUse of drug-killed cancer cells: A method to assess the therapeutic effectiveness of immunogenic cell death.
Methods Cell Biol
January 2025
Laboratorio de Inmunologia y Virologia, Facultad de Ciencias Biologicas, Universidad Autónoma de Nuevo Leon, San Nicolás de los Garza, Nuevo León, Mexico. Electronic address:
Cancer immunotherapy has revolutionized cancer treatment by harnessing the immune system's potential to combat cancer. Among the various strategies in this field, the use of killed tumor cells (KC) induced by immunogenic cell death (ICD) inducers has gained attraction. This approach involves the treatment of cancer cells in vitro, followed by the subcutaneous injection of these killed cells into tumor-bearing mice.
View Article and Find Full Text PDFSynthesis and functional screening of novel inhibitors targeting the HDAC6 zinc finger ubiquitin-binding domain.
Eur J Med Chem
December 2024
SynBioC Research Group, Department of Green Chemistry and Technology, Faculty of Bioscience Engineering, Ghent University, Ghent, Belgium; Cancer Research Institute Ghent (CRIG), Ghent, Belgium. Electronic address:
Histone deacetylase 6 (HDAC6) is a promising target for treating neurodegenerative disorders, several cancer types and viral infections. Unique among HDACs, the HDAC6 isoform possesses a zinc finger ubiquitin-binding domain (UBD) crucial for managing misfolded protein aggregates and facilitating viral infection. HDAC6 binds aggregated polyubiquitinated proteins through its UBD, mediating their transport to the aggresome and subsequent removal via autophagy.
View Article and Find Full Text PDFTargeting uPAR with an antibody-drug conjugate suppresses tumor growth and reshapes the immune landscape in pancreatic cancer models.
Sci Adv
January 2025
The Finsen Laboratory, Rigshospitalet, DK-2200 Copenhagen, Denmark.
Antibody-drug conjugates (ADCs) hold promise to advance targeted therapy of pancreatic ductal adenocarcinoma (PDAC), where the desmoplastic tumor stroma challenges effective treatment. Here, we explored the urokinase plasminogen activator receptor (uPAR) as a candidate ADC target in PDAC, harnessing its massive tumoral and stromal expression in this stroma-dense tumor. We generated a site-specific ADC offering high-affinity, cross-species reactivity, and efficient internalization of the anti-uPAR monoclonal antibody, FL1, carrying a potent anthracycline derivative (PNU-158692).
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