PBK/TOPK in the differential diagnosis of cholangiocarcinoma from hepatocellular carcinoma and its involvement in prognosis of human cholangiocarcinoma

He, Fengtian; Qu, Yan; Fan, Linni; Liu, Yixiong; Cui, Jihong; Wang, Juanhong; Wang, Lu; Wang, Yingmei; Wang, Zhe; Guo, Ying; Huang, Gaosheng

doi:10.1016/j.humpath.2009.05.016

Cited by 40 publications

(35 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, it is controversial whether TOPK affects cell proliferation. Some authors reported that TOPK expression did not affect cell proliferation [17,35], but others reported that high TOPK expression might promote cell proliferation [9,[11][12][13]. In our study, when TOPK expression was knocked down, cell proliferation was significantly inhibited in the MTT assay.…”

Section: Discussionmentioning

confidence: 42%

PBK/TOPK expression correlates with mutant p53 and affects patients' prognosis and cell proliferation and viability in lung adenocarcinoma

Lei

Zhao

et al. 2015

Human Pathology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 42%

PBK/TOPK expression correlates with mutant p53 and affects patients' prognosis and cell proliferation and viability in lung adenocarcinoma

Lei

Zhao

et al. 2015

Human Pathology

View full text Add to dashboard Cite

“…The PBK/TOPK gene is upregulated in various types of cancer and tumours such as bladder cancer, brain tumour, breast cancer, liver cancer, lung cancer and sarcoma (Park et al , 2006; Herrero-Martin et al , 2009; He et al , 2010; Shih et al , 2012; O Leary et al , 2013; Singh et al , 2014; Joel et al , 2015). PDZ-binding kinase/T-LAK cell-originated protein kinase was initially identified as a mitotic protein kinase (Gaudet et al , 2000), assisting the recruitment of cdk1/cyclin B to mitotic spindles, where PBK/TOPK plays a role in the formation of the spindle midzone and cytokinesis (Matsumoto et al , 2004).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of PBK/TOPK relates to tumour malignant potential and poor outcome of gastric carcinoma

et al. 2016

View full text Add to dashboard Cite

Background:PDZ-binding kinase/T-LAK cell-originated protein kinase (PBK/TOPK) is a serine–threonine kinase and overexpressed in various types of cancer by inhibiting the transactivation activities of p53 and PTEN. We tested whether PBK/TOPK acts as a cancer-promoting gene through its activation/overexpression in gastric cancer (GC).Methods:We analysed five GC cell lines and 144 primary tumours, which were curatively resected in our hospital between 2001 and 2003.Results:Overexpression of the PBK/TOPK protein was frequently detected in GC cell lines (4 out of 5 lines, 80.0%) was detected in primary tumour samples of GC (24 out of 144 cases, 16.6%) and was significantly correlated with venous invasion, tumour depth and recurrence rate. PDZ-binding kinase/T-LAK cell-originated protein kinase-overexpressing tumours had a worse survival rate than those with non-expressing tumours (P=0.0009, log-rank test). PDZ-binding kinase/T-LAK cell-originated protein kinase positivity was independently associated with a worse outcome in multivariate analysis (P<0.0001, hazard ratio 6.40 (2.71–14.49)). In PBK/TOPK-overexpressing GC cells, knockdown of PBK/TOPK inhibited the cell proliferation through the p53 activation in a TP53 mutation-dependent manner and inhibited the migration/invasion through the PTEN upregulation in a TP53 mutation-independent manner.Conclusions:These findings suggest PBK/TOPK plays a crucial role in tumour malignant potential through its overexpression and highlight its usefulness as a prognostic factor and potential therapeutic target in GC.

show abstract

“…The PBK/TOPK gene is up-regulated in various types of cancer and tumors such as bladder cancer, brain tumor, breast cancer, liver cancer, lung cancer and sarcoma (7)(8)(9)(23)(24)(25)(26). PBK/TOPK was initially identified as a mitotic protein kinase (27), assisting the recruitment of cylcin-dependent kinase 1 (CDK1)/cyclin B to mitotic spindles, where PBK/TOPK plays a role in the formation of the spindle midzone and cytokinesis (10).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of PBK/TOPK Contributes to Tumor Development and Poor Outcome of Esophageal Squamous Cell Carcinoma

Ohashi

Komatsu

Ichikawa

et al. 2016

View full text Add to dashboard Cite

Abstract. Background: PDZ-binding kinase/T-celloriginated protein kinase (PBK/TOPK) is a serine-threonine kinase and overexpressed in various types of cancer. PBK/TOPK is associated with tumor cell development and 58). Knockdown of PBK/TOPK using specific siRNAs inhibited the cell proliferation, invasion/migration of PBK/TOPK-overexpressing ESCC cell lines. Conclusion: These findings suggest that PBK/TOPK plays a crucial role in tumor malignant potential through its overexpression in ESCC.Esophageal cancer is the eighth most common cancer in the world (1) and esophageal squamous cell carcinoma (ESCC) accounts for 90% of esophageal carcinomas diagnosed in Asian countries. Although surgical techniques and perioperative management have progressed, ESCC remains one of the most aggressive carcinomas of the gastrointestinal tract. Since finding molecular targets for ESCC treatment might help improve the survival of patients with this lethal disease, studies have attempted to identify biological factors involved in the malignant potential of ESCC. However, few genes have been demonstrated to be associated with biological or pathological features of ESCC, suggesting that novel genes associated with the progression of ESCC need to be identified.Because identifying molecular targets for ESCC treatment may contribute to the improvement of survival of patients with this lethal disease, several recent studies have clarified that certain molecules, such as cyclo-oxygenase 2 (COX2), B-cell lymphoma (BCL2), tumor protein P53 (TP53), p16, cyclin D1, FAS, epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and E-cadherin (2-6), have important roles in tumorigenesis and the development of ESCC. Moreover, various genetic and epigenetic alterations that contribute to the carcinogenesis of ESCC have been elucidated. In clinical settings, however, only a few molecules have been validated as diagnostic, therapeutic, or prognostic biomarkers for ESCC. These findings prompted us to further search for novel cancerassociated molecules.PDZ binding kinase/T-LAK cell originated protein kinase (PBK/TOPK) encodes a serine/threonine protein kinase and is 6457

show abstract

PBK/TOPK in the differential diagnosis of cholangiocarcinoma from hepatocellular carcinoma and its involvement in prognosis of human cholangiocarcinoma

Cited by 40 publications

References 28 publications

PBK/TOPK expression correlates with mutant p53 and affects patients' prognosis and cell proliferation and viability in lung adenocarcinoma

PBK/TOPK expression correlates with mutant p53 and affects patients' prognosis and cell proliferation and viability in lung adenocarcinoma

Overexpression of PBK/TOPK relates to tumour malignant potential and poor outcome of gastric carcinoma

Overexpression of PBK/TOPK Contributes to Tumor Development and Poor Outcome of Esophageal Squamous Cell Carcinoma

Contact Info

Product

Resources

About