Aberrantly high CDC20 expression promotes tumour progression in bladder cancer, resulting in a poor prognosis, and may also constitute a promising therapeutic target.
Thus, this study identifies lidocaine as a potential anti-neoplastic agent for TNBC cells emphasizing CDC20 as a suitable therapeutic target for breast cancer. The online version contains supplementary material available at 10.1007/s13205-023-03554-7.
As an oncoprotein, Cdc20 is highly expressed in a variety of malignant tumors, and Cdc20 overexpression is associated with poor prognosis of these tumors. This review aims to dissect the tumorigenic role of Cdc20 in human malignancies and its targeting strategies.
Our study validates the essential role of p53 and CDC20 in MCL tumorigenesis, and provides a new insight for MCL therapeutics through dual-targeting p53 and CDC20.
Moreover, a positive correlation was noted between the high degree of infiltration with Th2 and CDC20. High expression of CDC20 predicted poor survival, as potential target in the treatment for HCC.
Generation of mice carrying the N331K variant using CRISPR-Cas9 showed that, while homozygous N331K mice were non-viable, heterozygotes displayed accelerated oncogenicity of Myc-driven cancers. These findings highlight an unappreciated role for CDC20 variants as tumor-promoting genes.
Overexpression of REC8 significantly inhibited the proliferation, migration and invasion of breast cancer cells in vitro; these changes were reversed by CDC20 overexpression. In conclusion, the present study demonstrated that REC8 decreased proliferation, migration and invasion of breast cancer cells by inhibiting CDC20.
Proapoptotic Bim accumulation was detected in our CDC20 inhibitor treated MDA-MB-468 cells. The most effective inhibitors, 22, warrant further development to target CDC20 in diseases.
miR-1321 and miR-7515 inhibited NSCLC development by targeting CDC20. Thus, the current study has implications in NSCLC treatment and provides novel insights into NSCLC management.
In summary, the synergy between MYBL2 and CDC20 induced the proliferation of GC cells and inhibited cell apoptosis; these effects may have involved the Wnt/β-catenin signaling pathway. Thus, MYBL2 may be a promising target for GC treatment.
Therefore, our studies delineated the oncogenic role of CDC20 and its prognostic significance at the pan-cancer level and proved its functional activity in Cdc20 high expression cancer types. Our studies will merits further molecular assays to understand the potential role of Cdc20 in tumorigenesis and provide the rationale for developing novel therapeutic strategies.
In conclusion, a five-gene signature (TOP2A, PCNA, AURKA, CDC20, CCNB2) overexpressed inHCC was identified, and a prognostic model was constructed. This gene signature may act as a prognostic model for HCC and provide potential targets of nanotechnology.
CDC20 alone could forecast HCC prognoses according to multivariable Cox regression analysis (hazard ratio=2.354, 95% confidence interval=1.177-4.709, P=0.016). CONCLUSIONS Overexpressed CDC20 may act as a reliable biomarker for dismal prognoses among HCC patients.
Moreover, overexpression of Cdc20 alleviated the inhibitory effects of Notch-1 downregulation on the viability, migration and invasion of OS cells. Our study offers a promising OS treatment strategy by inhibiting Notch-1.
Besides, targeting CDC20 was found to suppress tumorigenesis of DLBCL in vivo. CDC20 was identified as a key downstream gene of the MDM2-p53 signaling pathway in DLBCL and may be used as a novel target gene to guide therapeutic applications.
Furthermore, Bim and p21 were upregulated in OS cells following apcin treatment. Altogether, the results of the present study demonstrated that targeting CDC20 could be useful for the treatment of OS, and might be a promising solution for the treatment of the OS with cisplatin insensitivity.