scholarly journals Abnormal expressed long non-coding RNA IRAIN inhibits tumor progression in human renal cell carcinoma cells

2016 ◽  
Vol 11 (1) ◽  
pp. 200-205 ◽  
Author(s):  
Wang Zhiqiang ◽  
Liu Qian ◽  
Li Tieqiang ◽  
Li Xiaodong ◽  
Zhang Guangwei ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Cyclin D1 ◽  
Cell Lines ◽  
Renal Cell ◽  
Human Renal Cell Carcinoma ◽  
Non Coding Rna ◽  
Long Non Coding Rna

AbstractObjectivesThe long non-coding RNA (lncRNA) IRAIN has been verified to have key roles in tumor biology. The aim of this study was to explore its expression and biological functions in human renal cell carcinoma (RCC) cells.MethodsQuantitative RT-PCR was applied to detect the RNA expression of IRAIN in RCC tissues and cell lines when compared with respective controls. MTT and flow cytometry methods were respectively used to monitor the cell proliferation and apoptosis of 786-O cells after IRAIN was overexpressed. Altered expression of cyclin D1 and Bax was determined by immunoblotting. Xenograft models were finally carried out to confirm the roles of IRAIN in RCC in vivo.ResultsIRAIN expression was found to be remarkably decreased in RCC tissues and cell lines. Its overexpression in 786-O cells significantly inhibited cell proliferation and promoted apoptosis. We further demonstrated that cyclin D1 was reduced while apoptosis promoting protein Bax was elevated in IRAIN-overexpressed 786-O cells. Importantly, we found that IRAIN overexpression could suppress in vivo tumorigenesis of RCC, reflected by tumor volume and tumor weight measurement.ConclusionIRAIN might serve as a novel tumor suppressing lncRNA and a potential therapeutic target in RCC treatment.

scholarly journals Long Non-Coding RNA PANTR1 is Associated with Poor Prognosis and Influences Angiogenesis and Apoptosis in Clear-Cell Renal Cell Cancer

Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1200 ◽  
Author(s):  
Maximilian Seles ◽  
Georg C. Hutterer ◽  
Johannes Foßelteder ◽  
Marek Svoboda ◽  
Margit Resel ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Confidence Interval ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Renal Cell ◽  
Clear Cell ◽  
Kidney Tissue ◽  
Knock Down ◽  
Non Coding Rna ◽  
Long Non Coding Rna

POU3F3 adjacent non-coding transcript 1 (PANTR1) is an oncogenic long non-coding RNA with significant influence on numerous cellular features in different types of cancer. No characterization of its role in renal cell carcinoma (RCC) is yet available. In this study, PANTR1 expression was confined to human brain and kidney tissue and was found significantly up-regulated in clear-cell renal cell carcinoma tissue (ccRCC) compared to non-cancerous kidney tissue in two independent cohorts (p < 0.001 for both cohorts). In uni- and multivariate Cox regression analysis, ccRCC patients with higher levels of PANTR1 showed significantly poorer disease-free survival in our own respective cohort (n = 175, hazard ratio: 4.3, 95% confidence interval: 1.45–12.75, p = 0.008) in accordance with significantly poorer overall survival in a large The Cancer Genome Atlas database (TCGA) cohort (n = 530, hazard ratio: 2.19, 95% confidence interval: 1.59–3.03, p ≤ 0.001). To study the underlying cellular mechanisms mediated by varying levels of PANTR1 in kidney cancer cells, we applied siRNA-mediated knock-down experiments in three independent ccRCC cell lines (RCC-FG, RCC-MF, 769-P). A decrease in PANTR1 levels led to significantly reduced cellular growth through activation of apoptosis in all tested cell lines. Moreover, as angiogenesis is a critical driver in ccRCC pathogenesis, we identified that PANTR1 expression is critical for in vitro tube formation and endothelial cell migration (p < 0.05). On the molecular level, knock-down of PANTR1 led to a decrease in Vascular Endothelial growth factor A (VEGF-A) and cell adhesion molecule laminin subunit gamma-2 (LAMC2) expression, corroborated by a positive correlation in RCC tissue (for VEGF-A R = 0.19, p < 0.0001, for LAMC2 R = 0.13, p = 0.0028). In conclusion, this study provides first evidence that PANTR1 has a relevant role in human RCC by influencing apoptosis and angiogenesis.

scholarly journals SPOP Could Play a Potential Inhibitory Role in Human Renal Cell Carcinoma

2021 ◽  
Author(s):  
zhi chen ◽  
Zuan Li ◽  
Deyong Nong ◽  
Ximing Li ◽  
Guihai Huang ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Renal Cell ◽  
Immunohistochemical Staining ◽  
Human Renal Cell Carcinoma ◽  
Expression Levels ◽  
Normal Tissues ◽  
Proliferation And Apoptosis

Abstract Background: SPOP, a substrate adaptor of Cul3 ubiquitin ligase, plays crucial roles in solid neoplasms by promoting the ubiquitination and degradation of substrates. Limited studies have shown that SPOP is overexpressed in human renal cell carcinoma (RCC) tissue. However, the exact role of SPOP in RCC remains unclear and needs to be further elucidated. The present study showed that SPOP was expressed at different levels in different RCC cell lines. The purpose of this study was to explore the roles of SPOP in the biological features of RCC cells and determine the expression levels of SPOP in human tissue microarrays (TMAs) and kidney tissues.Methods: Here, SPOP was overexpressed by lentiviral vector transfection in ACHN and Caki-1 cells, and SPOP was knocked down in Caki-2 cells with similar transfection methods. The transfection efficiency was evaluated by quantitative PCR and western blotting analyses. The role of SPOP in the proliferation, migration, invasion and apoptosis of cell lines was determined by the MTT, wound-healing, Transwell and flow cytometry assays. Moreover, the cells were treated with different drug concentrations in proliferation and apoptosis assays to investigate the effect of sunitinib and IFN-α2b on the proliferation and apoptosis of SPOP-overexpressing cells and SPOP-knockdown RCC cells. Finally, immunohistochemical staining of SPOP was performed in kidney tissues and TMAs, which included RCC tissues and corresponding adjacent normal tissues.Results: Overexpression of SPOP inhibited cell proliferation, migration and invasion and increased cell apoptosis. Interestingly, sunitinib and IFN-α2b at several concentrations increased the proliferation inhibitory rate and total apoptosis rate of cells overexpressing SPOP. The findings of the present study showed that the SPOP protein was significantly expressed at low levels in most clear cell RCC (ccRCC) tissues and at relatively high levels in the majority of adjacent normal tissues and kidney tissues. Kaplan-Meier survival analysis showed that there was no statistically significant difference in cumulative survival based on the data of different SPOP expression levels in TMA and patients.Conclusions: In contrast to previous studies, our findings demonstrated that overexpression of SPOP might suppress the progression of RCC cells, which was supported by cell experiments and immunohistochemical staining. SPOP could be a potential tumour inhibitor in RCC.

scholarly journals Long non-coding RNA PTPRG-AS1 promotes cell tumorigenicity in epithelial ovarian cancer by decoying microRNA-545-3p and consequently enhancing HDAC4 expression

2020 ◽  
Author(s):  
Juanjuan Shi ◽  
Xijian Xu ◽  
Dan Zhang ◽  
Jiuyan Zhang ◽  
Hui Yang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Epithelial Ovarian Cancer ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Background: Long non-coding RNA PTPRG antisense RNA 1 (PTPRG-AS1) deregulation has been reported in various human malignancies and identified as an important modulator of cancer development. Few reports have focused on the detailed role of PTPRG-AS1 in epithelial ovarian cancer (EOC) and its underlying mechanism. This study aimed to determine the physiological function of PTPRG-AS1 in EOC. A series of experiments were also performed to identify the mechanisms through which PTPRG-AS1 exerts its function in EOC.Methods: Reverse transcription-quantitative polymerase chain reaction was used to determine PTPRG-AS1 expression in EOC tissues and cell lines. PTPRG-AS1 was silenced in EOC cells and studied with respect to cell proliferation, apoptosis, migration, and invasion in vitro and tumor growth in vivo. The putative miRNAs that target PTPRG-AS1 were predicted using bioinformatics analysis and further confirmed in luciferase reporter and RNA immunoprecipitation assays.Results: Our data verified the upregulation of PTPRG-AS1 in EOC tissues and cell lines. High PTPRG-AS1 expression was associated with shorter overall survival in patients with EOC. Functionally, EOC cell proliferation, migration, invasion in vitro, and tumor growth in vivo were suppressed by PTPRG-AS1 silencing. In contrast, cell apoptosis was promoted by loss of PTPRG-AS1. Regarding the mechanism, PTPRG-AS1 could serve as a competing endogenous RNA in EOC cells by decoying microRNA-545-3p (miR-545-3p), thereby elevating histone deacetylase 4 (HDAC4) expression. Furthermore, rescue experiments revealed that PTPRG-AS1 knockdown-mediated effects on EOC cells were, in part, counteracted by the inhibition of miR-545-3p or restoration of HDAC4.Conclusions: PTPRG-AS1 functioned as an oncogenic lncRNA that aggravated the malignancy of EOC through the miR-545-3p/HDAC4 ceRNA network. Thus, targeting the PTPRG-AS1/miR-545-3p/HDAC4 pathway may be a novel strategy for EOC anticancer therapy.

188 Development of a realistic in vivo bone metastasis model for human renal cell carcinoma

2014 ◽  
Vol 13 (1) ◽  
pp. e188
Author(s):  
M.P. Valta ◽  
H. Zhao ◽  
A. Ingels ◽  
A.E. Thong ◽  
R. Nolley ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Bone Metastasis ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Human Renal Cell Carcinoma ◽  
Metastasis Model
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