Upregulation of Protein Tyrosine Phosphatase Type IVA Member 3 (PTP4A3/PRL-3) is Associated with Tumor Differentiation and a Poor Prognosis in Human Hepatocellular Carcinoma

Mayinuer, Abudureheman; Yasen, Mahmut; Mogushi, Kaoru; Obulhasim, Gulanbar; Xieraili, Maimaiti; Aihara, Arihiro; Tanaka, Shinji; Mizushima, Hiroshi; Tanaka, Hiroshi; Arii, Shigeki

doi:10.1245/s10434-012-2395-2

Cited by 41 publications

(33 citation statements)

References 26 publications

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“…21 PTP4A3 may increase the potential for invasion by up-regulating MMP (matrix metalloproteinase) in colorectal cancer cell lines 22 and human hepatocellular carcinoma. 23 Taken together it is reasonable to consider PTP4A3 as an oncogene due to its numerous downstream effectors for oncogenesis. It is possible that the function of PTP4A3 is regulated by signals from the microenvironment and not universally identical in different cancer cells in light of the multiple pathways involved with PTP4A3.…”

Section: Discussionmentioning

confidence: 99%

PTP4A3 Independently Predicts Metastasis and Survival in Upper Tract Urothelial Carcinoma Treated with Radical Nephroureterectomy

Yeh

Huang

et al. 2015

Journal of Urology

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Section: Discussionmentioning

confidence: 99%

PTP4A3 Independently Predicts Metastasis and Survival in Upper Tract Urothelial Carcinoma Treated with Radical Nephroureterectomy

Yeh

Huang

et al. 2015

Journal of Urology

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“…The expression of PRL-3 is frequently upregulated in human tumors, such as breast cancer (21), liver cancer (22), ovarian cancer (23), gastric cancer (24), and colorectal cancer (25). This expression is associated with cancer progression and poor survival.…”

Section: Introductionmentioning

confidence: 99%

Ubiquitin-Specific Protease 4-Mediated Deubiquitination and Stabilization of PRL-3 Is Required for Potentiating Colorectal Oncogenesis

Xing

Guo

et al. 2016

Cancer Research

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Ubiquitin specific protease 4 (USP4) is a deubiquitinating enzyme with key roles in the regulation of p53 and TGFb signaling, suggesting its importance in tumorigenesis. However, the mechanisms and regulatory roles of USP4 in cancer, including colorectal cancer, remain largely elusive. Here, we present the first evidence that USP4 regulates the growth, invasion, and metastasis of colorectal cancer. USP4 expression was significantly elevated in colorectal cancer tissues and was significantly associated with tumor size, differentiation, distant metastasis, and poor survival. Knockdown of USP4 diminished colorectal cancer cell growth, colony formation, migration, and invasion in vitro and metastasis in vivo. Importantly, we found that phosphatase of regenerating liver-3 (PRL-3) is indispensable for USP4-mediated oncogenic activity in colorectal cancer.Mechanistically, we observed that USP4 interacted with and stabilized PRL-3 via deubiquitination. This resulted in activation of Akt and reduction of E-cadherin, critical regulators of cancer cell growth and metastasis. Examination of clinical samples confirmed that USP4 expression positively correlates with PRL-3 protein expression, but not mRNA transcript levels. Taken together, our results demonstrate that aberrant expression of USP4 contributes to the development and progression of colorectal cancer and reveal a critical mechanism underlying USP4-mediated oncogenic activity. These observations suggest that the potential of harnessing proteolytic degradation processes for therapeutic manipulation may offer a much-needed new approach for improving colorectal cancer treatment strategies. Cancer Res; 76(1); 83-95. Ó2015 AACR.

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“…This region also contains some cancer related genes such as PTP4A3 and PTK2 genes. The over expression of PTP4A3 has been reported in liver metastases derived from colorectal cancer as well as breast cancer, ovarian cancer, gastric cancer, esophageal carcinoma, and invasive cervical cancer [48]. This gene promotes the cell invasion and activity by stimulating of Rho signaling pathways [49].…”

Section: Discussionmentioning

confidence: 99%

A systematic comparison of copy number alterations in four types of female cancer

et al. 2016

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BackgroundDetection and localization of genomic alterations and breakpoints are crucial in cancer research. The purpose of this study was to investigate, in a methodological and biological perspective, different female, hormone-dependent cancers to identify common and diverse DNA aberrations, genes, and pathways.MethodsIn this work, we analyzed tissue samples from patients with breast (n = 112), ovarian (n = 74), endometrial (n = 84), or cervical (n = 76) cancer. To identify genomic aberrations, the Circular Binary Segmentation (CBS) and Piecewise Constant Fitting (PCF) algorithms were used and segmentation thresholds optimized. The Genomic Identification of Significant Targets in Cancer (GISTIC) algorithm was applied to the segmented data to identify significantly altered regions and the associated genes were analyzed by Ingenuity Pathway Analysis (IPA) to detect over-represented pathways and functions within the identified gene sets.Results and DiscussionAnalyses of high-resolution copy number alterations in four different female cancer types are presented. For appropriately adjusted segmentation parameters the two segmentation algorithms CBS and PCF performed similarly. We identified one region at 8q24.3 with focal aberrations that was altered at significant frequency across all four cancer types. Considering both, broad regions and focal peaks, three additional regions with gains at significant frequency were revealed at 1p21.1, 8p22, and 13q21.33, respectively. Several of these events involve known cancer-related genes, like PPP2R2A, PSCA, PTP4A3, and PTK2. In the female reproductive system (ovarian, endometrial, and cervix [OEC]), we discovered three common events: copy number gains at 5p15.33 and 15q11.2, further a copy number loss at 8p21.2. Interestingly, as many as 75% of the aberrations (75% amplifications and 86% deletions) identified by GISTIC were specific for just one cancer type and represented distinct molecular pathways.ConclusionsOur results disclose that some prominent copy number changes are shared in the four examined female, hormone-dependent cancer whereas others are definitive to specific cancer types.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2899-4) contains supplementary material, which is available to authorized users.

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Upregulation of Protein Tyrosine Phosphatase Type IVA Member 3 (PTP4A3/PRL-3) is Associated with Tumor Differentiation and a Poor Prognosis in Human Hepatocellular Carcinoma

Cited by 41 publications

References 26 publications

PTP4A3 Independently Predicts Metastasis and Survival in Upper Tract Urothelial Carcinoma Treated with Radical Nephroureterectomy

PTP4A3 Independently Predicts Metastasis and Survival in Upper Tract Urothelial Carcinoma Treated with Radical Nephroureterectomy

Ubiquitin-Specific Protease 4-Mediated Deubiquitination and Stabilization of PRL-3 Is Required for Potentiating Colorectal Oncogenesis

A systematic comparison of copy number alterations in four types of female cancer

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