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Review
. 2021 Apr 30;10(5):1073.
doi: 10.3390/cells10051073.

Myeloid-Derived Suppressor Cells as Therapeutic Targets in Uterine Cervical and Endometrial Cancers

Affiliations
Review

Myeloid-Derived Suppressor Cells as Therapeutic Targets in Uterine Cervical and Endometrial Cancers

Seiji Mabuchi et al. Cells. .

Abstract

Uterine cervical and endometrial cancers are the two most common gynecological malignancies. As demonstrated in other types of solid malignancies, an increased number of circulating or tumor-infiltrating myeloid-derived suppressor cells (MDSCs) have also been observed in uterine cervical and endometrial cancers, and increased MDSCs are associated with an advanced stage, a short survival, or a poor response to chemotherapy or radiotherapy. In murine models of uterine cervical and endometrial cancers, MDSCs have been shown to play important roles in the progression of cancer. In this review, we have introduced the definition of MDSCs and their functions, discussed the roles of MDSCs in uterine cervical and endometrial cancer progression, and reviewed treatment strategies targeting MDSCs, which may exhibit growth-inhibitory effects and enhance the efficacy of existing anticancer treatments.

Keywords: MDSC; ovarian cancer; survival; therapeutic target; tumor microenvironment.

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Figure 1
Figure 1
Immune suppression by myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment. Immune suppression by MDSCs is mainly antigen-specific, contact-dependent, and utilizes several major pathways, such as (a) production of reactive oxygen (ROS) and reactive nitrogen species (nitric oxide (NO) or peroxynitrite (PNT)); (b) elimination of L-arginine or L-tryptophan, key nutrition factors for T cells, from the tumor microenvironment by the production of arginase-1 or indoleamine-2,3-dioxygenase (IDO), respectively; (c) disruption of homing of T cells (through the expression of ADAM17); (d) production of immunosuppressive cytokines (transforming growth factor (TGF)-β, interleukin [IL]-10); and (e) induction of T regulatory (Treg) cells.

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