학술논문

Respiratory complex I regulates dendritic cell maturation in explant model of human tumor immune microenvironment.
Document Type
article
Source
Journal for ImmunoTherapy of Cancer. 12(4)
Subject
Breast Neoplasms
Dendritic Cells
Drug Evaluation
Preclinical
Immunity
Innate
Immunomodulation
Humans
Female
Electron Transport Complex I
Antineoplastic Agents
Breast Neoplasms
Dendritic Cells
Metformin
Tumor Microenvironment
Sulfonamides
Bridged Bicyclo Compounds
Heterocyclic
Language
Abstract
BACKGROUND: Combining cytotoxic chemotherapy or novel anticancer drugs with T-cell modulators holds great promise in treating advanced cancers. However, the response varies depending on the tumor immune microenvironment (TIME). Therefore, there is a clear need for pharmacologically tractable models of the TIME to dissect its influence on mono- and combination treatment response at the individual level. METHODS: Here we establish a patient-derived explant culture (PDEC) model of breast cancer, which retains the immune contexture of the primary tumor, recapitulating cytokine profiles and CD8+T cell cytotoxic activity. RESULTS: We explored the immunomodulatory action of a synthetic lethal BCL2 inhibitor venetoclax+metformin drug combination ex vivo, discovering metformin cannot overcome the lymphocyte-depleting action of venetoclax. Instead, metformin promotes dendritic cell maturation through inhibition of mitochondrial complex I, increasing their capacity to co-stimulate CD4+T cells and thus facilitating antitumor immunity. CONCLUSIONS: Our results establish PDECs as a feasible model to identify immunomodulatory functions of anticancer drugs in the context of patient-specific TIME.