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  • br Fig CDCA is upregulated in breast cancer


    Fig. 5. CDCA8 is upregulated in breast cancer and increased CDCA8 expression predicts poor prognosis in breast carcinoma patients. (A) IHC analysis of CDCA8 expression in breast cancer tissues. (B) RT-PCR analysis CDCA8 in breast cancer tissues. GAPDH served as loading control. (C) Kaplan-Meier's analysis of the correlation between CDCA8 expression and overall survival of breast cancer patients. Data were shown as mean ± S.D. of three independent experiments. **p < 0.01.
    migration, and invasion (Ci et al., 2019) and decrease the proliferation of human embryonic stem cells (Marko et al., 2014).
    As an essential regulator of mitosis, some reports indicate that CDCA8 is found to be especially over-expressed in triple negative breast cancers (Jiao et al., 2015), while others point that CDCA8 has a high expression level in invasive lobular breast carcinoma, male breast car-cinoma, and invasive ductal breast carcinoma subtypes (Phan et al., 2018). In this study, the expression of CDCA8 is found to be correlated with the tumor size of the breast cancer patient. Furthermore, both present investigation and previous analysis (Jiao et al., 2015) reveal that the expression of CDCA8 is significantly associated with patient prognosis and CDCA8 can be utilized as an independent prognostic factor. Thus, all of these data suggest the potential treatment option of CDCA8 in these subtypes.
    ERα is vital in the pathogenesis and clinical behavior of breast cancer. In this investigation, CDCA8 knockdown can influence well-known ERα-induced genes, such as CCND1 and BCL2 (Tozlu et al., 2006). As a well-established human oncogene and a member of the cyclins (J R et al., 2000), CCND1 is important in 329-98-6 regulation and temporal coordination of each mitotic event (Elizabeth et al., 2011; Beà and Amador, 2017), which is over-expressed in breast cancer (Fereshteh et al., 2013) and such over-expression is associated with poor patient progress (Katunarić et al., 2014). BCL2 is an integral outer mitochondrial membrane protein that blocks the apoptotic death, whose up-regulation can promote tumorigenesis and tumor progression and is related to worse outcome (Tsujimoto et al., 1984; Radha and Raghavan, 2017). All of these indicate that CDCA8 might be an im-portant downstream factor in residual amounts of E2 induced ERα signal pathway.
    In this research, P21 and P27 are testified to be up-regulated by CDCA8 knockdown, which could inhibit cyclin E-CDK2 and cyclin D-CDK4 complexes activation, and thus arrest the cell cycle progression at G1. It is worth noting that growing evidence indicates that functional loss of p21 or p27 can mediate a drug-resistance phenotype, while some  Gene 703 (2019) 1–6
    research also reports that p21 and p27 can promote carcinogenesis, indicating a paradoxical effect. All in all, this research suggests that CDCA8 could act as the main downstream molecule of residual amounts of E2 stimulation, which will have a high potency to target Tamoxifen-resistant breast cancer.
    5. Conclusion
    CDCA8 can be considered to be a promising target for novel ther-apeutics of breast cancers.
    Disclosure of potential conflicts of interest
    The authors declare that they have no conflict of interest.
    Not applicable.
    Appendix A. Supplementary data
    Marko, N.F., Weil, R.J., Schroeder, J.L., Lang, F.F., Dima, S., Sawaya, R.E., 2014. Extent of resection of glioblastoma revisited: personalized survival modeling facilitates more accurate survival prediction and supports a maximum-safe-resection approach to surgery. J. Clin. Oncol. 32, 774–782.
    Tozlu, S., Girault, I., Vacher, S., Vendrell, J., Andrieu, C., Spyratos, F., Cohen, P., Lidereau, R., Bieche, I., 2006. Identification of novel genes that co-cluster with es-trogen receptor alpha in breast tumor biopsy specimens, using a large-scale real-time reverse transcription-PCR approach. Endocr. Relat. Cancer 13, 1109–1120.
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    Research paper
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    b Department of Pathology, Affiliated Putian Hospital of Putian College, Fujian, China
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