Increased PTOV1 expression is related to poor prognosis in epithelial ovarian cancer

Guo, Fei; Liu, Feng; Hu, Ji-Long; Wang, Meiling; Luo, Peng; Zhong, Xiaoming; Deng, Anmei

doi:10.1007/s13277-014-2662-x

Cited by 13 publications

(14 citation statements)

References 14 publications

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“…A strong nuclear staining was more frequently found in the T3 or T4 stage and metastatic cancer cells; from the clinical data, we also found a correlation between PTOV1 overexpression and ESCC clinical progression. Similar to other findings, 12,13,15 PTOV1 overexpression had a strong relationship with the tumor size and T staging. Moreover, IHC staining showed that the intensity of PTOV1 expression in the ESCC tissues increased with progressing clinical stage and lymph node involvement, and all these collectively indicated that the elevated expression of PTOV1 lead to a more aggressive character.…”

Section: Discussionsupporting

confidence: 89%

Overexpressed PTOV1 associates with tumorigenesis and progression of esophageal squamous cell carcinoma

Leng

Liu

et al. 2017

Tumour Biol.

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PTOV1 has been demonstrated to play an extensive role in many types of cancers. This study takes the first step to clarify the potential relationship between esophageal squamous cell carcinoma and PTOV1 expression and highlight the link between PTOV1 and the tumorigenesis, progression, and prognosis of esophageal squamous cell carcinoma. PTOV1 expression was detected by quantitative reverse transcription polymerase chain reaction and western blotting or immunohistochemical staining in esophageal squamous cell carcinoma cell lines, esophageal squamous cell carcinoma tissues, and its paired adjacent non-cancerous tissues. Moreover, we have analyzed the relationship between PTOV1 expression and clinicopathological features of esophageal squamous cell carcinoma. Survival analysis and Cox regression analysis were used to assess its prognostic significance. We found that PTOV1 expression was significantly higher in the esophageal squamous cell carcinoma cell lines and tissues at messenger RNA level (p < 0.001) and protein level (p < 0.001). Gender, tumor size, or differentiation was tightly associated with the PTOV1 expression. Lymph node involvement (p < 0.001) and TNM stage (p < 0.001) promoted a high PTOV1 expression. A prognostic significance of PTOV1 was also found by Log-rank method, and the overexpression of PTOV1 was related to a shorter OS and DFS. Multiple Cox regression analysis indicated overexpressed PTOV1 as an independent indicator for adverse prognosis. In conclusion, this study takes the lead to demonstrate that the overexpressed PTOV1 plays a vital role in the tumorigenesis and progression of esophageal squamous cell carcinoma, and it is potentially a valuable prognostic predicator and new chemotherapeutic target for esophageal squamous cell carcinoma.

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Section: Discussionsupporting

confidence: 89%

Overexpressed PTOV1 associates with tumorigenesis and progression of esophageal squamous cell carcinoma

Leng

Liu

et al. 2017

Tumour Biol.

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“…Consistently, this study also showed that PTOV1 increases the proportion of SP cells, which can exclude the DNA-binding dye Hoechst 33342, suggesting that PTOV1 may enhance the chemoresistance of breast cancer cells. Although numerous studies have elucidated the significance of PTOV1 in a variety of tumours [3,21,33,34], this is the first report of a role for PTOV1 in the stemness of cancer cells. Thus, our findings not only reveal a novel mechanism for the maintenance of CSCs in breast cancer but also represent a novel target for restraining the CSC population in breast cancer.…”

Section: Discussionmentioning

confidence: 81%

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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“…PTOV1 was initially identified in prostate cancer, but it has recently been reported to enhance the population of cancer stem cells via the activation of Wnt/β-catenin signaling in breast cancer (15). PTOV1 is also a key player in tumor progression and is associated with a poor prognosis in laryngeal squamous cell carcinoma, urothelial carcinoma, and ovarian cancer (16–18). In addition to the oncogenic roles of its sense transcripts, our findings strongly suggest that antisense PTOV1-AS1 is also involved in cancer proliferation via miR-1207-5p.…”

Section: Discussionmentioning

confidence: 99%

hnRNPK-regulated PTOV1-AS1 modulates heme oxygenase-1 expression via miR-1207-5p

2017

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Antisense transcripts were initially identified as transcriptional noise, but have since been reported to play an important role in the quality control of miRNA functions. In this report, we tested the hypothesis that heterogeneous nuclear ribonucleoprotein K (hnRNPK) regulates miRNA function via competitive endogenous RNAs, such as pseudogenes, long non-coding RNAs, and antisense transcripts. Based on analyses of RNA sequencing data, the knockdown of hnRNPK decreased the antisense PTOV1-AS1 transcript which harbors five binding sites for miR-1207-5p. We identified heme oxygenase-1 (HO-1) mRNA as a novel target of miR-1207-5p by western blotting and Ago2 immunoprecipitation. The knockdown of hnRNPK or PTOV1-AS1 suppressed HO-1 expression by increasing the enrichment of HO-1 mRNA in miR-1207-5p-mediated miRISC. Downregulation of HO-1 by a miR-1207-5p mimic or knockdown of hnRNPK and PTOV1- AS1 inhibited the proliferation and clonogenic ability of HeLa cells. Taken together, our results demonstrate that hnRNPK-regulated PTOV1-AS1 modulates HO-1 expression via miR-1207-5p.

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Increased PTOV1 expression is related to poor prognosis in epithelial ovarian cancer

Cited by 13 publications

References 14 publications

Overexpressed PTOV1 associates with tumorigenesis and progression of esophageal squamous cell carcinoma

Overexpressed PTOV1 associates with tumorigenesis and progression of esophageal squamous cell carcinoma

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

hnRNPK-regulated PTOV1-AS1 modulates heme oxygenase-1 expression via miR-1207-5p

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