Overexpression of Cdc20 in clinically localized prostate cancer: Relation to high Gleason score and biochemical recurrence after laparoscopic radical prostatectomy

Mao, Yunfei; Li, Ke; Li, Lu; Song, Jie; Lu, Minhua; Gao, Xin

doi:10.3233/cbm-160573

Cited by 32 publications

(26 citation statements)

References 33 publications

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“…It has previously been reported that Cdc20 overexpression is associated with the occurrence of glioblastomas, while Cdc20 downregulation occurs in patients with low-grade tumors (15). Recently, Mao et al (16) demonstrated that Cdc20 overexpression may serve as an independent predictor of biochemical recurrence in patients with clinically localized prostate cancer undergoing laparoscopic radical prostatectomy without neoadjuvant therapy. Furthermore, Cdc20 upregulation was reported to be associated with poor prognosis in urothelial bladder (17), uterine cervix (18), colorectal cancer (19), pancreatic ductal adenocarcinoma (20), oral squamous cell carcinoma (21), gastric (22) and lung cancer (23).…”

Section: Introductionmentioning

confidence: 99%

Cdc20 inhibitor apcin inhibits the growth and invasion of osteosarcoma cells

et al. 2018

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Osteosarcoma (OS) is the most common primary malignant bone tumor worldwide, primarily affecting children and adolescents. The anaphase promoting complex/cyclosome (APC/C) is a ubiquitin ligase that is activated by its co‑activator Cdc20 during the metaphase‑anaphase transition. Apcin is a novel cell‑permeable molecule that blocks the interaction between APC/C and Cdc20. Cdc20 overexpression has been reported in various malignancies and plays an oncogenic role in tumorigenesis and tumor progression. In the present study, the antitumor properties of apcin, an inhibitor of Cdc20, was investigated in OS cell lines. In addition, the possible molecular target by which apcin mediates cell death was explored. Apcin was demonstrated to inhibit OS cell growth and induce significant apoptosis. The invasion and mobile abilities of OS cells were also markedly suppressed by apcin treatment. Furthermore, Bim and p21 were upregulated in OS cells following apcin treatment. The results of the present study indicated that apcin may have therapeutic potential as a treatment for OS and that Cdc20 may be a promising molecular target for chemotherapy.

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Section: Introductionmentioning

confidence: 99%

Cdc20 inhibitor apcin inhibits the growth and invasion of osteosarcoma cells

et al. 2018

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“…Moreover, it is estimated that there would be 161,360 new prostate cancer diagnoses and 26,730 prostate cancer-associated mortalities in 2015 (1,2). The molecular heterogeneity of prostate cancer can make its early diagnosis and treatment problematic; thus, the identification of accurate molecular biomarkers and potential therapeutic targets (at various disease stages) may result in improved patient outcome (3,4). It is therefore important to investigate the molecular mechanisms underpinning the development and progression of prostate cancer, as this may catalyze the identification of novel therapeutic targets (5,6).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of contactin‑1 expression promotes prostate cancer progression

et al. 2019

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Contactin-1 (CNTN-1) has been reported to serve an oncogenic role in several cancer types. However, detailed mechanisms describing the influence of CNTN-1 in prostate cancer progression have not yet been elucidated. The present study aimed to determine the clinical significance of CNTN-1 expression in prostate cancer progression, and also to investigate the regulatory role of CNTN-1 in the proliferation, migration and invasive ability of prostate cancer cells. The results of the present study indicated that expression levels of CNTN-1 were significantly higher in prostate cancer tissues compared with adjacent normal tissues. Moreover, a high expression level of CNTN-1 was positively correlated with tumor size, stage and metastasis, as well as a poorer prognosis in patients with prostate cancer. Furthermore, CNTN-1-knockdown in prostate cancer cells (using short hairpin RNA) resulted in the significant inhibition of cancer cell proliferation, colony formation, migration and invasiveness. Silencing of CNTN-1 expression also suppressed epithelial-mesenchymal transition in prostate cancer cells via the upregulation of E-cadherin, and the downregulation of N-cadherin and vimentin expression. Inhibition of CNTN-1 expression also reduced the activity of the PI3K/AKT signaling pathway in prostate cancer cells. Thus, it was demonstrated that CNTN-1 expression is upregulated, and plays an oncogenic role, in prostate cancer cells. The results of the current study suggest that CNTN-1 may represent a promising therapeutic target, potentially improving the treatment of patients with prostate cancer.

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“…The BPH tissues and PCa tissues were respectively from patients treated by transurethral resection of prostate and laparoscopic radical prostatectomy in the Third Affiliated Hospital of Sun Yat-sen University during 1st January 2012 and 31st December 2015. IHC was performed as described previously [18]. Briefly, tissues were deparaffinized and then antigen retrieval was done in 10 mmol/L citrate buffer (pH 6.0) for 15 min at 100 °C.…”

Section: Methodsmentioning

confidence: 99%

Identification of endonuclease domain-containing 1 as a novel tumor suppressor in prostate cancer

et al. 2017

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BackgroundEndonuclease domain containing 1 (ENDOD1) is implicated in tumorigenesis and aggressiveness of multiple tumors. In this study, we aimed to investigate the role of ENDOD1 in prostate cancer (PCa).MethodsImmunohistochemistry were performed in 30 cases of benign prostatic hyperplasia (BPH) and 50 cases of PCa to identify its association with clinicopathological characteristics. Real-time PCR and western blot were used to detect ENDOD1 mRNA and protein expression in normal prostatic epithelial and PCa cell lines. MTT assays were employed to determine the effect of cell proliferation. Flow cytometry was used to explore the cell cycle distribution and apoptotic effects. Transwell migration and invasion assays were done to evaluate changes in the ability of cell migration and invasion.ResultsImmunoreactivity scores of ENDOD1 showed no statistical difference between BPH and low-grade PCa, whereas lower immunostaining scores were observed in high-grade compared with low-grade PCa. Real-time PCR data indicated that ENDOD1 mRNA expression was markedly increased in LNCaP and 22Rv1 cells and decreased in PC3 and DU145 cells compared to the normal epithelial cells RWPE1. Western blot showed that androgen-sensitive LNCaP cells had the highest protein expression level of ENDOD1, whereas castration-resistant PCa cell lines PC3 and DU145 had significantly lower protein levels. Meanwhile, overexpression of ENDOD1 suppressed cell proliferation, induced G0/G1 cell cycle arrest and inhibited cell migration and invasion. Conversely, siRNA-mediated silencing of ENDOD1 promoted cell proliferation, migration and invasion. No apoptotic effects occurred upon manipulation of ENDOD1 expression.ConclusionOur results indicate that ENDOD1 is a novel tumor suppressor in PCa, which may be employed as a new drug target of preventing progression to metastatic castration-resistant prostate cancer.

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Overexpression of Cdc20 in clinically localized prostate cancer: Relation to high Gleason score and biochemical recurrence after laparoscopic radical prostatectomy

Abstract: Overexpression of Cdc20 may serve as an independent predictor for BCR in patients of clinically localized PCa undergoing LRP without neoadjuvant therapy.

Cited by 32 publications

References 33 publications

Cdc20 inhibitor apcin inhibits the growth and invasion of osteosarcoma cells

Cdc20 inhibitor apcin inhibits the growth and invasion of osteosarcoma cells

Upregulation of contactin‑1 expression promotes prostate cancer progression

Identification of endonuclease domain-containing 1 as a novel tumor suppressor in prostate cancer

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