Image_1_Upregulation of CCT-3 Induces Breast Cancer Cell Proliferation Through miR-223 Competition and Wnt/β-Catenin Signaling Pathway Activation.TIF
The clinical significance and the function of chaperonin-containing TCP1 complex 3 (CCT-3) in breast cancer remain unknown. In this study, we found that CCT-3 was markedly overexpressed in breast cancer tissues. Statistical analysis revealed a significant correlation of CCT-3 expression with advanced breast cancer clinical stage and poorer survival. Ablation of CCT-3 knocked down the proliferation and the tumorigenicity of breast cancer cells in vitro and in vivo. CCT-3 may regulate breast cancer cell proliferation through a ceRNA network between miR-223 and β-catenin, thus affecting Wnt/β-catenin signaling pathway activation. We also validated that CCT-3 and β-catenin are novel direct targets of tumor suppressor miR-223. Our results suggest that both mRNA and the protein levels of CCT-3 are potential diagnosis biomarkers and therapeutic targets for breast cancer.
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References
- https://doi.org//10.3322/caac.20107
- https://doi.org//10.1158/1538-7445.SABCS18-PD3-02
- https://doi.org//10.1073/pnas.1620451114
- https://doi.org//10.1002/path.2056
- https://doi.org//10.1002/jso.21625
- https://doi.org//10.3748/wjg.v21.i28.8588
- https://doi.org//10.1111/apm.12258
- https://doi.org//10.1016/j.yexcr.2015.02.005
- https://doi.org//10.1002/pmic.201800157
- https://doi.org//10.1038/s41598-019-47895-x
- https://doi.org//10.1093/carcin/bgz137
- https://doi.org//10.1001/jama.2010.1525
- https://doi.org//10.1200/JOP.777003
- https://doi.org//10.5858/arpa.2013-0953-SA
- https://doi.org//10.1002/1097-0142(20001215)89:12<2637::AID-CNCR17>3.0.CO;2-B
- https://doi.org//10.1093/nar/gkq1056
- https://doi.org//10.1093/nar/gkt1248
- https://doi.org//10.1007/s10549-009-0674-9
- https://doi.org//10.1016/j.ccell.2019.07.002
- https://doi.org//10.1016/j.ctrv.2017.11.002
- https://doi.org//10.1136/jmedgenet-2015-103334
- https://doi.org//10.1038/s41571-019-0253-x
- https://doi.org//10.1371/journal.pbio.1001844
- https://doi.org//10.1016/j.celrep.2014.09.056
- https://doi.org//10.1016/S0092-8674(00)00122-7
- https://doi.org//10.1146/annurev.cellbio.20.010403.113126
- https://doi.org//10.1158/1078-0432.CCR-06-2316
- https://doi.org//10.1016/j.gendis.2018.05.001
- https://doi.org//10.1038/nsmb.1515
- https://doi.org//10.1007/978-94-007-4186-7_3
- https://doi.org//10.1080/15548627.2019.1598750
- https://doi.org//10.1002/jcsm.12374
- https://doi.org//10.1016/j.ejcb.2015.05.010
- https://doi.org//10.2147/OTT.S217019
- https://doi.org//10.1038/onc.2016.23
- https://doi.org//10.1158/0008-5472.CAN-19-1793
- https://doi.org//10.1073/pnas.1222509110
- https://doi.org//10.1038/onc.2013.106
- https://doi.org//10.1016/j.biopha.2013.06.006
- https://doi.org//10.1371/journal.pone.0084859