期刊
JOURNAL OF TRANSLATIONAL MEDICINE
卷 20, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s12967-022-03494-5
关键词
Castration-resistant prostate cancer (CRPC); Prostate cancer (PCa); Myeloid-Derived suppressor cells (MDSCs); Exosomes; Circular RNAs (circRNAs); miR-506-3p
资金
- Scientific Research Foundation of Zhejiang Province Traditional Chinese Medicine Administration Bureau [2018ZQ036]
- Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province [2020E10021]
This study identified a S100A9/circMID1/miR-506-3p/MID1 axis in MDSC-Exo-regulated CRPC progression, providing new insights into the regulatory mechanisms of MDSC-Exo in CRPC progression.
Background Castration-resistant prostate cancer (CRPC) is a major cause of recurrence and mortality among prostate cancer (PCa) patients. Myeloid-derived suppressor cells (MDSCs) regulate castration resistance in PCa. Previously, it was shown that intercellular communication was efficiently mediated by exosomes (Exos), but the role and the mechanism of MDSC-derived Exos in CRPC progression was unclear. Methods In this study, the circRNA expression profiles in PC3 cells treated with MDSC-Exo and control cells were investigated using a circRNA microarray. Results The data showed that circMID1 (hsa_circ_0007718) expression was elevated in PC3 cells treated with MDSC-Exo. Moreover, high circMID1 expression was found in PCa compared with benign prostatic hyperplasia (BPH) tissues and in CRPC patients compared with hormone sensitive prostate cancer (HSPC) patients. Further studies showed that MDSC-Exo accelerated PCa cell proliferation, migration, and invasion, while circMID1 deficiency inhibited MDSC-Exo-regulated CRPC progression in vitro and in vivo. Mechanistically, MDSC-derived exosomal S100A9 increased circMID1 expression to sponge miR-506-3p, leading to increased MID1 expression and accelerated tumor progression. Conclusion Together, our results showed that a S100A9/circMID1/miR-506-3p/MID1 axis existed in MDSC-Exo-regulated CRPC progression, which provided novel insights into MDSC-Exo regulatory mechanisms in CRPC progression.
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