Overexpression of prostate tumor overexpressed 1 correlates with tumor progression and predicts poor prognosis in breast cancer

Lei, Fangyong; Zhang, Longjuan; Li, Xinghua; Lin, Xi; Wu, Shu; Li, Fengyan; Liu, Junling

doi:10.1186/1471-2407-14-457

Cited by 18 publications

(21 citation statements)

References 24 publications

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“…Based on our observations and other studies, we hypothesize that PTOV1 may coordinate with other factors, such as CBX7, to modulate the balance between DKK1 promoter histone acetylation and deacetylation, and thereby control the cellular expression of DKK1. However, the balance of this system is broken by overexpression of PTOV1 in breast cancer, as reported in our previous study , and thus leads to decreased expression of DKK1 and subsequent hyperactivation of Wnt/β‐catenin signalling.…”

Section: Discussionsupporting

confidence: 65%

“…Moreover, PTOV1 regulates gene expression by altering histone acetylation . We previously reported that PTOV1 is highly expressed in breast cancer and is associated with poorer patient prognosis, indicating a significant role for PTOV1 in breast cancer . In this study, we demonstrate that PTOV1 contributes to maintenance of the CSC population and promotes tumourigenicity in breast cancer through activation of the Wnt/β‐catenin pathway.…”

Section: Introductionsupporting

confidence: 60%

“…Our previous study revealed that high‐level expression of PTOV1 was associated with a poor prognosis in breast cancer, suggesting that PTOV1 may be involved in the regulation of breast cancer development and progression . Since CSCs have been demonstrated to drive tumour initiation and malignant progression, and are closely associated with a poor clinical outcome, we investigated the role of PTOV1 in the maintenance of the CSC‐like phenotype.…”

Section: Resultsmentioning

confidence: 99%

“…Immunohistochemistry was performed as described previously . After deparaffinization, the sections were immunohistochemically stained using anti‐PTOV1 (SAB1303504, 1:100; Sigma), anti‐β‐catenin antibody (#8480, 1:200; Cell Signaling, Danvers, MA, USA), and anti‐DKK1 (3435–1, 1:300; Epitomics) primary antibodies.…”

Section: Methodsmentioning

confidence: 99%

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Prostate tumour overexpressed-1 promotes tumourigenicity in human breast cancer via activation of Wnt/β-catenin signalling

Cui

Lei

et al. 2016

J. Pathol.

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Breast cancer is the most common malignancy in females. The presence of cancer stem cells (CSCs) is the main cause of local and distant tumour recurrence and is associated with poor outcome in breast cancer. However, the molecular mechanisms underlying the maintenance of CSCs remain largely unknown. This study demonstrates that prostate tumour overexpressed-1 (PTOV1) enhances the CSC population and augments the tumourigenicity of breast cancer cells both in vitro and in vivo. Moreover, PTOV1 suppresses transcription of Dickkopf-1 (DKK1) by recruiting histone deacetylases and subsequently reducing DKK1 promoter histone acetylation, followed by activation of Wnt/β-catenin signalling. Restoration of DKK1 expression in PTOV1-overexpressing cells counteracts the effects of PTOV1 on Wnt/β-catenin activation and the CSC population. Collectively, these results suggest that PTOV1 positively regulates the Wnt/β-catenin signalling pathway and enhances tumourigenicity in breast cancer; this novel mechanism may represent a therapeutic target for breast cancer. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

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Section: Discussionsupporting

confidence: 65%

Section: Introductionsupporting

confidence: 60%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Prostate tumour overexpressed-1 promotes tumourigenicity in human breast cancer via activation of Wnt/β-catenin signalling

Cui

Lei

et al. 2016

J. Pathol.

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“…Overexpression of PTOV1 promotes tumor progression and is a predictor of poor prognosis in breast cancer [51]. Also, PTOV1 promotes the tumorigenicity by activating Wnt/β-catenin pathway in breast cancer [52].…”

Section: Discussionmentioning

confidence: 99%

Silencing of the CSNK2β gene by siRNA inhibits invasiveness and growth of MDA-MB-231 cells

Karna

Lone

Ahmad

et al. 2018

Preprint

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Background: Breast cancer is most common cancer and accounts for one-fourth of all cancer diagnoses worldwide. Treatment of triple-negative breast cancer is major challenge and identification of specific drivers is required for targeted therapies. The aim of our present study is to elucidate the therapeutic potential of CSNK2β silencing in triple negative breast cancer MDA-MB-231 cell.Methods: CSNK2β gene has been knockdown using siRNA and silencing was estimated by both real time and western blot. Cell Titer-Glo (CTG) and colony formation assay and wound healing assay, cell cycle analysis by flow cytometry was performed to assess the role of CSNK2β in cell proliferation, migration, cell cycle, and oncogenesis.Morphological assessment of nuclear condensation, apoptosis by Hoechst staining and measurement of intracellular ROS production was examined using fluorescence microscopy. Real time PCR and western blot was done to study the expression of genes related to cell proliferation, survival, metastasis, apoptosis, and autophagy.Results: Silencing of CSNK2β in MDA-MB-231 cells resulted in decreased cell viability, colony formation, and migratory potential. Cell cycle analysis showed that growth inhibitory effect was mediated by arresting the cells in G2/M phase. Furthermore, we demonstrated that silencing of CSNK2β increased the nuclear condensation and intracellular ROS production. CSNK2β regulates the expression of BAX, Bcl-xL, caspase 3, Beclin-1, LC3-I, p-ERK, p38-α, c-Myc, MAPK, c-Jun, NF-κB, β -catenin, E2F1, PCNA. We have also shown the functional relationship between CSNK2β, PIN1, and PTOV1 by western blotting. We have first time reported that silencing CSNK2β using siRNA can inhibit invasiveness and proliferation of MDA-MB-213 cells. Conclusion:Our results suggested that CSNK2β silencing may offer future therapeutic target in triple negative breast cancer. BackgroundCasein Kinase 2(CSNK2), a highly conserved, multifunctional serine/threonine protein kinase, is critically important for the regulation of different processes in eukaryotes, such as proliferation, differentiation, and apoptosis [1-3]. CSNK2 is ubiquitously expressed in all tissues but its level is elevated in tumor tissues including prostate [4], mammary gland [5], head and neck [6], lungs [7] and kidney [8]. CSNK2 possess a heterotetrameric conformation with two catalytic and two regulatory subunits [9].CSNK2β supports the structure of the tetrameric complex, augments catalytic activity and stability of CSNK2 and can also function dependently with other catalytic subunits [10][11][12][13]9].In a mammalian cell, CSNK2β is phosphorylated at Ser 209 at its autophosphorylation site and at Ser 53B, in a cell cycle-dependent manner and in vitro by p34 cdc5 [14,15].CSNK2β is responsible for recruitment of CSNK2 substrates or potential regulators such as Nopp140, p53, Fas-associated factor-1 (FAF-1), topoisomerase II, CD5 and fibroblast growth factor-2 (FGF-2) [16][17][18][19][20][21][22]. Yeast two-hybrid interaction showed that CSNK2β interact with ...

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Prostate tumor overexpressed 1 expression in invasive urothelial carcinoma

Rausch

Hennenlotter

Scharpf

et al. 2016

J Cancer Res Clin Oncol

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Subcellular distribution seems to be the most important feature of PTOV1 expression in UC. Nuclear localization of PTOV1 along with cytoplasmic decrease in PTOV1 expression was identified as putative surrogate for PTOV1-associated cellular proliferation and dedifferentiation in UC. The functional relevance as well as the potential role of PTOV1 as a biomarker in UC remains to be specified in future studies.

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Overexpression of prostate tumor overexpressed 1 correlates with tumor progression and predicts poor prognosis in breast cancer

Cited by 18 publications

References 24 publications

Prostate tumour overexpressed-1 promotes tumourigenicity in human breast cancer via activation of Wnt/β-catenin signalling

Prostate tumour overexpressed-1 promotes tumourigenicity in human breast cancer via activation of Wnt/β-catenin signalling

Silencing of the CSNK2β gene by siRNA inhibits invasiveness and growth of MDA-MB-231 cells

Prostate tumor overexpressed 1 expression in invasive urothelial carcinoma

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