Speckle-type POZ protein is negatively associated with malignancies and inhibits cell proliferation and migration in liver cancer

Huang, Yuping; Tan, Nguan Soon; Jia, Deshui; Jing, Ying; Wang, Qifeng; Li, Zhe; Zhang, Jiwei; Liu, Li; Li, Jinjun; Chen, Zhiao; He, Xianghuo

doi:10.1007/s13277-015-3753-z

Cited by 19 publications

(13 citation statements)

References 30 publications

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“… 23 Similarly, SPOP has also been reported to inhibit the proliferation and migration of liver cancer cells. 24 On the contrary, the results of the colony formation assay in the current study indicated that silencing SPOP inhibited the colony formation ability. The trans-well migration assay also indicated that silencing SPOP attenuated the migration ability of the RCC cells.…”

Section: Discussioncontrasting

confidence: 67%

RNA interference-mediated silencing of speckle-type POZ protein promotes apoptosis of renal cell cancer cells

Liu

Sun

2016

OTT

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This study aimed to investigate the effects of silencing the speckle-type POZ protein (SPOP) gene on renal cell cancer (RCC) cells and to explore its possible mechanism. The A498 and ACHN RCC cells were transfected with small interference RNA (siRNA)-SPOP by lipofection methods. The silencing efficiency was monitored by quantitative real-time polymerase chain reaction and Western blot. The effects of SPOP silencing on cell apoptosis, cell viability, colony formation ability, cell migration ability, and chemosensitivity to Sorafenib were assessed by flow cytometry, an MTT assay, a colony formation assay, a trans-well migration assay, and a CCK-8 assay, respectively. Its effects on the expression of several cytokines were determined by a protein microarray. Relevant signaling pathways were also analyzed. Compared with the control group, the cell apoptosis rate was significantly higher; the cell viability, the colony formation, and migration ability were significantly decreased in the siRNA-SPOP group. The protein microarray screening showed that the expression of vascular endothelial growth factor receptor, matrix metallopeptidase-9, vascular cell adhesion molecule-1, and stromal cell-derived factor-1 in the siRNA group was significantly decreased and that the expression of granulocyte–macrophage colony-stimulating factor and E-cadherin was significantly increased (P<0.05). The relevant signaling pathways were the integrin-mediated cell surface interactions pathway and extracellular matrix organization signal pathway. SPOP gene silencing induced cell apoptosis, decreased cell viability, colony formation, and migration ability, and elevated the drug sensitivity in the RCC cells. A possible mechanism is that silencing SPOP induces the differential expression of E-cadherin, vascular endothelial growth factor receptor, matrix metallopeptidase-9, and vascular cell adhesion molecule, which are related to the integrin-mediated cell surface interactions and extracellular matrix organization signaling pathway.

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Section: Discussioncontrasting

confidence: 67%

RNA interference-mediated silencing of speckle-type POZ protein promotes apoptosis of renal cell cancer cells

Liu

Sun

2016

OTT

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“…Although HB and HCC are the most common malignant pediatric liver tumors and are characterized by aggressive growth and early metastasis, the molecular mechanisms underlying their development remain largely unknown [38]. Numerous oncogenic molecules and signaling pathways are co-regulated by functionally-related TFs and associated genes [39].…”

Section: Discussionmentioning

confidence: 99%

GATA4 promotes hepatoblastoma cell proliferation by altering expression of miR125b and DKK3

et al. 2016

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GATA4 is a zinc finger DNA-binding protein that plays an important role in mammalian liver development. However, the effects of GATA4 in hepatoblastoma (HB), a common liver cancer in pediatric patients, remain largely unknown. In this study, we demonstrate that GATA4 promotes growth and survival in the Huh6 human hepatoblastoma cell line. GATA4 expression was high in Huh6 cells, and its knockdown decreased expression of Dickkopf-related protein 3 (DKK3), a gene that may contribute to premature or undifferentiated phenotypes in HB. GATA4 also directly bound to the promoter regions of the miRNA miR125b and inhibited its expression in Huh6 cells. DKK3 was a direct target of miR125b in Huh6 cells. Inhibition of miR125b or overexpression of DKK3 promoted proliferation, survival, migration, and invasion in Huh6 cells. This is the first report to demonstrate that GATA4 promotes oncogenesis by inhibiting miR125b-dependent suppression of DKK3 expression. This GATA4/miR125b/DKK3 axis may be a major regulator of growth, migration, invasion, and survival in hepatoma cells, and is therefore a potential therapeutic target or biomarker for progression in HB patients.

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“…As a common malignant tumor among tumors of children, the prognosis of hepatoblastoma is often related to the type of disease differentiation. Although many genes and pathways have been studied in HB, the speci c molecular mechanism has not been revealed 22 . It has been demonstrated that the miR-100/let-7a-2/miR-125b-1 cluster works with miR-371-3 in HB.…”

Section: Discussionmentioning

confidence: 99%

MiR-125b-5p Inhibited The Progression of Hepatoblastoma As A Shared miRNA of The lncRNA NEAT1 and YES1

Jin

Chen

Mao

et al. 2020

Preprint

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Background: microRNAs have been studied widely in hepatoblastoma. However, the role of miR-125b-5p and its relationship with the lncRNA sNEAT1 and YES1 in hepatoblastoma have not been reported previously. We aimed to reveal the role of NEAT1/miR-125b-5p/YES1 in the progression of hepatoblastoma.Methods: We collected tumor tissues and their adjacent tissues from 12 hepatoblastoma patients. qRT-PCR was applied to detect the expression of miR-125b-5p, and the relationship of miR-125b-5p with clinicopathological characteristics was analyzed. Dual luciferase reporter assays and RNA pull down assays were used to identify the relationships among NEAT1, miR-125b-5p and YES1. CCK8, Transwell assays and wound healing assays were used to examine cell viability, invasion and migration. In vivo experiments were also applied to detect the effect of miR-125b-5p on hepatoblastoma.Results: miR-125b-5p was significantly downregulated in hepatoblastoma tissue and cells. The higher the PRETEXT grade, the lower the miR-125b-5p level. NEAT1 could bind to miR-125b-5p and inhibit its expression. miR-125b-5p could target YES1 and inhibit its expression. Overexpression of miR-125b-5p decreased the proliferation, invasion, and migratory ability of hepatoblastoma cells. YES1 could rescue the above effects. At the same time, overexpression of miR-125b-5p resulted in decreased YES1 and tumor growth inhibition in vivo.Conclusion: miR-125b-5p acted as a shared miRNA of NEAT1 and YES1 in hepatoblastoma. Overexpression of miR-125b-5p could target YES1 and inhibit its expression, therefore inhibiting the progression of hepatoblastoma.

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Speckle-type POZ protein is negatively associated with malignancies and inhibits cell proliferation and migration in liver cancer

Cited by 19 publications

References 30 publications

RNA interference-mediated silencing of speckle-type POZ protein promotes apoptosis of renal cell cancer cells

RNA interference-mediated silencing of speckle-type POZ protein promotes apoptosis of renal cell cancer cells

GATA4 promotes hepatoblastoma cell proliferation by altering expression of miR125b and DKK3

MiR-125b-5p Inhibited The Progression of Hepatoblastoma As A Shared miRNA of The lncRNA NEAT1 and YES1

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