Neobavaisoflavone inhibits antitumor immunosuppression via myeloid-derived suppressor cells
•Neobavaisoflavone inhibited the growth of 4T1 tumor in vivo.•Neobavaisoflavone attenuated tumor progression by targeting MDSCs.•Neobavaisoflavone suppresses the expansion and suppressive function of MDSCs.•Neobavaisoflavone decreases MDSCs in a STAT3 dependent manner.•Neobavaisoflavone enhanced the...
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Published in | International immunopharmacology Vol. 111; p. 109103 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Elsevier B.V
01.10.2022
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Subjects | |
Online Access | Get full text |
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Summary: | •Neobavaisoflavone inhibited the growth of 4T1 tumor in vivo.•Neobavaisoflavone attenuated tumor progression by targeting MDSCs.•Neobavaisoflavone suppresses the expansion and suppressive function of MDSCs.•Neobavaisoflavone decreases MDSCs in a STAT3 dependent manner.•Neobavaisoflavone enhanced the anti-PD-1efficiency in anti-PD-1 insensitive 4T1 tumor.
Neobavaisoflavone (Neo), as a traditional Chinese medicine, is the active ingredient in the herb Psoralea corylifolial and has antitumor activity. Myeloid-derived suppressor cells (MDSCs), which are a heterogeneous population of haematopoietic cells of the myeloid lineage, have been reported to be closely related to the pathogenesis of tumour progression, but whether Neo can regulate MDSC expansion and function remains unclear. Here, we found that Neo could inhibit the expansion and suppressive function of MDSCs by targeting STAT3. Importantly, Neo inhibited the growth of 4T1 and LLC tumours in vivo, as well as lung metastasis of 4T1 tumours in vivo. Furthermore, we identified MDSCs as the direct targets by which Neo attenuated tumour progression. In addition, Neo notably enhanced anti-PD-1 efficacy in anti-PD-1-insensitive 4T1 tumours. Therefore, our study sheds light on the development of Neobased therapeutic strategies against cancer. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1567-5769 1878-1705 |
DOI: | 10.1016/j.intimp.2022.109103 |