SCIENCE@home

CD39+MDSC facilitates cisplatin resistance of ovarian cancer cells by affecting adenosine synthesis.

Jiong Ma,Chunxia Zhou,Xia Zheng,Xuejun Chen

Published 2023 in Current pharmaceutical design

ABSTRACT

BACKGROUND Chemoresistance is a major cause of relapse or death in ovarian cancer (OC) patients. New evidence suggests the crucial role of myeloid-derived suppressor cells (MDSCs) in mediating chemoresistance of cancer cells. We aimed to dissect the way MDSCs affect the cisplatin resistance phenotype of OC and the related mechanisms. METHODS MDSCs were isolated from the spleen of OC mice isograft. CCK-8 and colony formation assays revealed the effects of an MDSC-conditioned medium with dysregulated CD39 on the proliferation and cisplatin sensitivity of OC cells. Fluorescence assay was used to reveal the effects of MDSCs with dysregulated CD39 on adenosine triphosphate (ATP) hydrolysis and adenosine (ADO) synthesis. RESULTS MDSCs with highly expressed CD39 could facilitate the proliferation and cisplatin resistance of OC cells, while MDSCs with downregulated CD39 caused the opposite results. In addition, MDSCs with upregulated CD39 could facilitate the hydrolysis of immunogenic ATP to immunosuppressive ADO, while the introduction of CD39 inhibitor could repress such hydrolysis of ATP and generation of ADO, thereby abating the proliferation and cisplatin resistance of OC cells. CONCLUSION CD39+MDSC could promote the proliferation and cisplatin resistance of OC cells by generating high concentrations of ADO, which indicates that targeting CD39+MDSC might be a feasible way to improve cisplatin resistance in OC.

PUBLICATION RECORD

CITATION MAP

EXTRACTION MAP

CLAIMS

  • No claims are published for this paper.

CONCEPTS

  • No concepts are published for this paper.

REFERENCES

Showing 1-25 of 25 references · Page 1 of 1

CITED BY