The relationship between the expression of USP22, BMI1, and EZH2 in hepatocellular carcinoma and their impacts on prognosis

Zhai, Run; Tang, Fang; Gong, Jianhua; Zhang, Jing; Lei, Biao; Li, Bo; Wei, Yangchao; Liang, Xingsi; Tang, Bo; He, Songqing

doi:10.2147/ott.s110985

Cited by 25 publications

(22 citation statements)

References 26 publications

(24 reference statements)

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“…We found USP22 silencing led to decreased expression of BMI1, as well as decreased P21 levels. Meanwhile, EZH2, another Polycomb-group (PcG) protein associated with histone modification of H3K27me3 (Figure 6C), showed no change in abundance, consistent with a study reporting that USP22 silencing did not change EZH2 in hepatocellular carcinoma [29]. Our results also confirmed that USP22 silencing caused increased ubH2A expression (Figure 6C), in accordance with a previous report demonstrating that ubH2A was a substrate of USP22 [14].…”

Section: Resultssupporting

confidence: 92%

USP22 maintains gastric cancer stem cell stemness and promotes gastric cancer progression by stabilizing BMI1 protein

Wang

et al. 2017

Oncotarget

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Increased ubiquitin-specific protease 22 (USP22) has been associated with poor prognosis in several cancers including gastric cancer. However, the role of USP22 in gastric tumorigenesis is still unclear. Gastric cancer stem cells have been identified and shown to correlate with gastric cancer initiation and metastasis. In this study, we found that silencing of USP22 inhibited proliferation of gastric cancer cells and suppressed the cancer stem cell spheroid formation in serum-free culture. Furthermore, cancer stem cell markers, such as CD133, SOX2, OCT4 and NANOG were down-regulated. Additionally, knockdown of USP22 inhibited gastric cancer xenografts growth. Our analysis of TCGA database indicated that BMI1 overexpression may predict gastric cancer patient survival, and TAT-BMI1 proteins reversed the USP22 knockdown-mediated decreased in cancer stem cell properties, and elevated the expression of stemness-associated genes. Furthermore, we found that overexpression of USP22 stabilized the BMI1 protein in gastric cancer cells. Taken together, our study demonstrates that USP22 is indispensable for gastric cancer stem cell self-renewal through stabilization of BMI1. These results may provide novel approaches to the theranostics of gastric cancer in the near future.

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Section: Resultssupporting

confidence: 92%

USP22 maintains gastric cancer stem cell stemness and promotes gastric cancer progression by stabilizing BMI1 protein

Wang

et al. 2017

Oncotarget

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“…For example, EZH2 promotes cell proliferation in laryngeal carcinoma [ 16 ], inducing cell metastasis in oral cancer [ 17 ], increasing cell invasion in endometrial cancer [ 18 ] Dysregulation of EZH2 in HCC has been found in some studies. For instance, up-regulated EZH2 was measured in HCC tissues, which was positively correlated with tumor grade and clinical stage [ 19 ]. Cheng et al found that downregulation of EZH2 inhibited HCC cell growth through inhibition of β-catenin signaling [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA PVT1 modulates hepatocellular carcinoma cell proliferation and apoptosis by recruiting EZH2

Jian-ping¹,

Hao

Wang

et al. 2018

Cancer Cell Int

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BackgroundWe aimed to figure out the molecular network of PVT1 and EZH2 on hepatocellular carcinoma (HCC) cells growth. We also explored the interaction between PVT1, EZH2, MDM2 and P53.MethodsMicroarray analysis was performed to screen for abnormally expressed genes in HCC tissues and PVT1 was identified as one gene significantly upregulated in HCC. CCK-8 assay, colony formation assay, and flow cytometry detected cell vitality, proliferation and apoptosis, respectively. RIP and RNA pull-down assays were employed to examine the connection between PVT1 and EZH2. The effect of PVT1 on the stability of EZH2 protein and the impact of EZH2 on MDM2 were detected by ELISA. Co-immunoprecipitation assay was used to evaluate the relationship between MDM2 and EZH2. Western blot detected the expression of EZH2, MDM2 and P53.ResultsUp-regulated PVT1 was detected in HCC. Knockdown of PVT1 inhibited HCC cell propagation and promoted apoptotic cells. PVT1 could improve EZH2 protein stability by binding to EZH2 protein but have no significant impact on EZH2 mRNA expression. EZH2 protein stabilized MDM2 protein expression by binding to MDM2 protein. PVT1 enhanced the protein expression of EZH2 and MDM2 as well as inhibited P53 protein expression.ConclusionsPVT1 promoted HCC cell propagation and inhibited apoptotic cells by recruiting EZH2, stabilizing MDM2 protein expression and restraining P53 expression.Electronic supplementary materialThe online version of this article (10.1186/s12935-018-0582-3) contains supplementary material, which is available to authorized users.

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“…It has been found that EZH2 is a core component of the family of Polycomb group proteins ( 3 ). Studies have shown that EZH2 has abnormal expression in gastric ( 4 ), esophageal ( 5 ), liver cancer ( 6 , 7 ) and other malignant tumors and is closely related to tumor growth, development and prognosis. However, there has been very little research on the expression of EZH2 protein in the tissues of patients with EC.…”

Section: Introductionmentioning

confidence: 99%

Expression of EZH2 in endometrial carcinoma and its effects on proliferation and invasion of endometrial carcinoma cells

Zhang

Huai

2017

Oncol Lett

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Expression of enhancer of zeste homolog 2 (EZH2) has been implicated in cancer pathology, but research on its mechanistic activity is limited. The present study sought to assess the levels expression of EZH2 in patients with endometrial carcinoma (EC) and to explore the effects of EZH2 downregulation on the biological behavior of endometrial carcinoma RL-952 cells. Samples were obtained from a total of 104 patients with EC and an immunohistochemical assay was used to detect the expression of EZH2 in cancer and adjacent tissues. The relationship between the expression of EZH2 and the clinicopathological features was analyzed. Endometrial carcinoma RL-952 cells were transfected with chemically synthesized siRNA to conduct targeting inhibition of EZH2 expression. The expression levels of EZH2 protein were detected by immunoblotting. MTT and Transwell assays were used to detect the changes of cell proliferation and invasion after EZH2 downregulation. Of the 104 cases of endometrial carcinoma samples, 71 cases showed positive expression of EZH2, with an expression rate of 68.27%. In 104 cases of adjacent tissue samples, 25 cases showed positive expression of EZH2, with an expression rate of 24.03%. The expression of EZH2 in endometrial carcinoma tissue was significantly higher than that in adjacent tissue (P<0.05). The expression of EZH2 in endometrial carcinoma tissue was not correlated with the menopausal status and age of patients (P>0.05), but was correlated with the histological grade, depth of tumor invasion, lymph node metastasis and TNM stage (P<0.05). The expression of E2H2 was significantly downregulated by si-E2H2 and the proliferation and invasion abilities of cells were significantly reduced after EZH2 downregulation (P<0.05). EZH2 is closely related to the development of endometrial carcinoma and can enhance the proliferative activity of endometrial carcinoma RL-952 cells and promote cell invasion.

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The relationship between the expression of USP22, BMI1, and EZH2 in hepatocellular carcinoma and their impacts on prognosis

Cited by 25 publications

References 26 publications

USP22 maintains gastric cancer stem cell stemness and promotes gastric cancer progression by stabilizing BMI1 protein

USP22 maintains gastric cancer stem cell stemness and promotes gastric cancer progression by stabilizing BMI1 protein

Long noncoding RNA PVT1 modulates hepatocellular carcinoma cell proliferation and apoptosis by recruiting EZH2

Expression of EZH2 in endometrial carcinoma and its effects on proliferation and invasion of endometrial carcinoma cells

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