Knockdown of Cdc25B in Renal Cell Carcinoma is Associated with Decreased Malignant Features

Yu, Xiuyue; Zhang, Zhe; Zhang, Guojun; Guo, Kun-Feng; Kong, Chuize

doi:10.7314/apjcp.2012.13.3.931

Cited by 18 publications

(15 citation statements)

References 19 publications

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“…CDC25B plays a minor role in the pathogenesis and/or progression of vulvar carcinoma, which has been associated with malignant features and aggressive cancer phenotypes but not independently correlated to prognosis 20. In contrast, we have identified that the expression of CDC25B was increased distinctively in carcinoma over that in the adjacent normal tissues, at both mRNA and protein levels, and there was a positive correlation between CDC25B expression and clinical stage and histopathologic grade of RCC 21. However, the mechanism that leads to the dysregulation of CDC25B within the specific context of tumor proliferation and progression has largely remained elusive.…”

Section: Discussionmentioning

confidence: 62%

MicroRNA-141 is downregulated in human renal cell carcinoma and regulates cell survival by targeting CDC25B

Yu¹,

Zhang²,

Liu³

et al. 2013

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Background/objectiveMicroRNAs (miRNAs) are small noncoding RNAs (ribonucleic acids), approximately 22 nucleotides in length, that function as regulators of gene expression. Dysregulation of miRNAs has been associated with the initiation and progression of oncogenesis in humans. The cell division cycle (CDC)25 phosphatases are important regulators of the cell cycle. Their abnormal expression detected in a number of tumors implies that their dysregulation is involved in malignant transformation.MethodsUsing miRNA target prediction software, we found that miR-141 could target the 3′ untranslated region (3′UTR) sequence of CDC25B. To shed light on the role of miR-141 in renal cell carcinogenesis, the expression of miR-141 was examined by real-time polymerase chain reaction (RT-PCR) in renal cell carcinoma and normal tissues. The impact of miR-141 re-expression on 769-P cells was analyzed using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and colony-forming assay. A luciferase reporter assay was applied to prove the functionality of the miR-141 binding site.ResultsmiR-141 is significantly downregulated in renal cell carcinoma. miR-141 re-expression suppressed cell growth in 769-P cells. Luciferase expression from a reporter vector containing the CDC25B-3′UTR was decreased when this construct was transfected with miR-141 in 769-P cells. The overexpression of miR-141 suppressed the endogenous CDC25B protein level in 769-P cells.ConclusionFor the first time, we demonstrated that CDC25B is a direct target of miR-141 in renal cell carcinoma. The transcriptional loss of miR-141 and the resultant increase in CDC25B expression facilitates increased genomic instability at an early stage of renal cell carcinoma development.

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Section: Discussionmentioning

confidence: 62%

MicroRNA-141 is downregulated in human renal cell carcinoma and regulates cell survival by targeting CDC25B

Yu¹,

Zhang²,

Liu³

et al. 2013

OTT

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“…Li et al (2011) found that high expression of CXC receptor 4 (CXCR4) was associated with not only increased risk for disease progression, but also worse OS of high-risk LARCC patients. Yu et al (2012) proved that knockdown of cdc25B in ccRCC is associated with decreased malignant features and cdc25B was an attractive prognostic marker for this tumor. Some other biomarkers were also found to be promising molecular predictor of tumor recurrence, such as RNA-binding protein IMP3 (Jiang et al, 2006), carbonic anhydrase 9 (Tostain et al, 2010), and P53 .…”

Section: Discussionmentioning

confidence: 95%

“…Once metastasis occurred, the patients with metastatic ccRCC would face a poor prognosis with a median survival of 6-10 months and a 10-20% 2-year survival rate (Janzen et al, 2003). In recent years, some prognostic markers for ccRCC, such as RALYL (Cui et al, 2012), CXCR4 (Li et al, 2011), Cdc25B (Yu et al, 2012), have appeared, but large-scale clinical application is impossible. Despite the continual progress in medical technology, the clinical characteristic of ccRCC is still difficult to predict (Wei et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

TGF-β-activated Kinase-1: A Potential Prognostic Marker for Clear Cell Renal Cell Carcinoma

Wei

Lai²,

Li³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Background: TGF-β-activated kinase-1 (TAK1) has been found to be over-expressed in a variety of solid malignancies and related to tumor growth. The aim of this study was to evaluate the expression level of TAK1 in clear cell renal cell carcinoma (ccRCC) and assess its value as a novel prognostic marker. Methods: TAK1 mRNA was assessed in 51 paired ccRCC tissues and adjacent normal tissues (ADTs) by real-time PCR. Tissue TAK1 protein was also assessed in 91 ADTs and 177 samples of ccRCC immunohistochemically for evaluation of relationships with clinical characteristics. Results: RT-PCR showed that TAK1 RNA level was significantly higher in ccRCC tissues than in the paired ADTs and immunohistochemistry confirmed higher expression of TAK1 protein in ccRCC samples compared with ADTs. TAK1 protein expression in 177 ccRCC samples was significantly correlated with T stage, N classification, metastasis, recurrence and Fuhrman grade, but not age and gender. Patients with low TAK1 levels had a better survival outcome. TAK1 expression and N stage were independent prognosis factors for the overall survival of ccRCC patients. Conclusions: Overexpression of TAK1 predicts a poor prognosis in patients with ccRCC, so that TAK1 may serve as a novel prognostic marker.

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“…Downregulation of CDC25B in renal cancer cells causes G2/M arrest, and subsequently induces cell apoptosis with concomitant reduction of the 14‐3‐3 protein. CDC25B knockdown is associated with a decrease in malignant features; for example, cancer cell migration and invasion . Furthermore, a selective inhibitor of CDC25 phosphatases; that is, Cpd5, might have potential as an anti‐neoplastic agent for RCC …”

Section: Pps In Genitourinary Cancermentioning

confidence: 99%

Role of protein phosphatases in genitourinary cancers

Igawa

2016

Int J of Urology

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The prevalence of genitourinary cancers has been increasing rapidly worldwide over the past 10 years. Advances in diagnosis and treatment have improved the oncological outcomes of patients with genitourinary cancer. However, the precise mechanisms of cancer development are largely unknown. Among various biological mechanisms, reversible phosphorylation is crucial for regulating the activities of many proteins in cancer cells. In contrast to protein kinases, the roles of cellular protein phosphatases have not been fully elucidated. However, emerging evidence suggests that various protein phosphatases are involved in genitourinary cancer development and have potential for cancer treatment. In the present review, we focus on recent progress in protein phosphatases regarding genitourinary cancers. We also explore the development of new strategies for cancer therapy using protein phosphatase and related molecules.

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Knockdown of Cdc25B in Renal Cell Carcinoma is Associated with Decreased Malignant Features

Cited by 18 publications

References 19 publications

MicroRNA-141 is downregulated in human renal cell carcinoma and regulates cell survival by targeting CDC25B

MicroRNA-141 is downregulated in human renal cell carcinoma and regulates cell survival by targeting CDC25B

TGF-β-activated Kinase-1: A Potential Prognostic Marker for Clear Cell Renal Cell Carcinoma

Role of protein phosphatases in genitourinary cancers

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