Work

FOXO3-dependent suppression of PD-L1 promotes anticancer immune responses via activation of natural killer cells.

Year: 2022

Type: article

Abstract: . SN38 treatment also promotes tumor cell apoptosis in the TME. SN38 treatment significantly decreases STAT3-pY705 and IL-6 protein levels; FOXO3 is essential for SN38-mediated PD-L1 downregulation. Collectively, these findings may contribute to future translational or clinical investigations tackling difficult-to-treat cancers with immune-activating medicines or combined with ICB immunotherapy.

Source: PubMed Central

Authors: Young Min Chung, Wen Bin Tsai, Pragya P Khan, Jessica Ma, Jonathan S Berek, James W Larrick, Mickey C-T Hu

Institutions: Stanford Medicine, Panorama Research (United States), Stanford University, The University of Texas MD Anderson Cancer Center

Language: English

Topic: Cancer Immunotherapy and Biomarkers

Subfield: Oncology

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: green

Funder: National Institutes of Health

Awards: Developing Novel Therapies for Treating Breast-Cancer-Related Lymphedema, Stem Cell-Adrenomedullin Therapy for Cancer Linked Lymphedema

OpenAlex ID: W4225795182

FWCI: 0.522

Cites: 76

Cited by: 5

Related to: 10