scholarly journals Roles of transcriptional factor Snail and adhesion factor E-cadherin in clear cell renal cell carcinoma

2013 ◽  
Vol 6 (6) ◽  
pp. 1489-1493 ◽  
Author(s):  
JINQUAN CAI
2007 ◽  
Vol 87 (12) ◽  
pp. 1252-1264 ◽  
Author(s):  
Michelle L Gervais ◽  
Pauline C Henry ◽  
Arthy Saravanan ◽  
T Nadine Burry ◽  
Brenda L Gallie ◽  
...  

2017 ◽  
Vol 64 (3) ◽  
pp. 465-470 ◽  
Author(s):  
Małgorzata Borzym-Kluczyk ◽  
Iwona Radziejewska ◽  
Marzanna Cechowska-Pasko ◽  
Barbara Darewicz

2021 ◽  
Author(s):  
Qingqing Zhou ◽  
Jiajun Li ◽  
Chao Ge ◽  
Jinsi Chen ◽  
Wei Tian ◽  
...  

Abstract Background: Aberrant expression of SNX5 can contribute to tumourigenesis, invasion, and metastasis of several human cancers. However, the clinicopathological and biological significance of SNX5 in clear cell renal cell carcinoma (ccRCC) remain unclear. The aim of this study was to examine the role of SNX5 in the progression of ccRCC.Methods: Immunohistochemical (IHC), Western blot, qRT-PCR, western blot, flow cytometry and immunofluorescence were used to detect the expression of indicated molecules. The biological role of SNX5 in ccRCC cells was evaluated by CCK8, colony formation, transwell assay, subcutaneous tumor formation as well as veil tail injection. ChIP assay and luciferase reporter assay were used to determine the direct binding of KLF9 to the promoter of the SNX5 gene.Results: SNX5 expression was downregulated in human ccRCC tissues. SNX5 expression was negatively correlated with tumor size, AJCC stage, tumor thrombus of inferior vena cava (IVC) and poor prognosis of ccRCC. Ectopic expression of SNX5 inhibited ccRCC cell proliferation and metastasis whereas knockdown of SNX5 increase these activities both in vitro and in vivo. Mechanistically, overexpression of SNX5 blocked internalization and intracellular trafficking of CD44 in ccRCC cells. Exogenous expression of CD44 partially rescued the inhibitory effects of SNX5 on the proliferation and invasion activity of ccRCC cells. Knockdown of SNX5 in ccRCC cells was associated with epithelial mesenchymal transition (EMT), including the down-regulation of E-cadherin, ZO-1 and Claudin-1 and the concomitant up-regulation of Snail and N-cadherin. In addition, SNX5 inhibited TGF-β-induced migration, invasion and EMT in ccRCC cells. Moreover, we observed a significant correlation between SNX5 expression and E-cadherin levels in ccRCC patients. In addition, KLF9 directly bound to the SNX5 promoter and increased SNX5 transcription. SNX5 expression was closely correlated with KLF9 expression in ccRCC. Moreover, we found that the combination of SNX5 and CD44 or E-cadherin or KLF9 was a more powerful predictor of poor prognosis than either parameter alone.Conclusion: Collectively, our data reveal a mechanism that KLF9-mediated SNX5 expression was associated with poor prognosis via trafficking of CD44 and promoting EMT in ccRCC. SNX5 may be a potential prognostic biomarker and therapeutic target for patients with ccRCC.


2018 ◽  
Vol 25 (4) ◽  
pp. 335-345 ◽  
Author(s):  
Ola A. Harb ◽  
Mariem A. Elfeky ◽  
Basant Sh El Shafaay ◽  
Heba F. Taha ◽  
Gamal Osman ◽  
...  

Author(s):  
Zongtao Ren ◽  
Yunfeng Niu ◽  
Bo Fan ◽  
Aili Zhang

Abstract Background Clear cell renal cell carcinoma (CCRCC) is one of the most common types of renal cell carcinoma. Accumulating evidence indicates that homeobox D10 (HOXD10) acts as a tumor suppressor or oncogene in various carcinomas. However, the regulation and potential mechanisms of HOXD10 in CCRCC remain largely unknown. Purpose To explore the effect and potential mechanism of HOXD10 on the invasion and migration of CCRCC cells. Methods The expression of HOXD10, E-cadherin and other epithelial mesenchymal transition (EMT)-related proteins was assessed by reverse transcription-quantitative real-time PCR (qRT-PCR) and Western blots. A series of functional assays were performed in RCC cell lines to explore the function of HOXD10 in CCRCC progression. Bioinformatics analysis, ChIP assays, and dual luciferase reporter assays were utilized to identify the interaction between HOXD10 and E-cadherin. Results Low expression of HOXD10 and E-cadherin was observed in CCRCC tissues and ACHN and 786-O cells. Downregulation of HOXD10 expression was correlated with the TNM stage of CCRCC patients. Functional experiments demonstrated that malignant biological ability was significantly inhibited by HOXD10 overexpression in RCC cells. Moreover, E-cadherin was a potential target gene of HOXD10, as evidenced by a series of assays. In addition, overexpression of HOXD10 inhibited the progression of CCRCC by regulating the expression of E-cadherin, vimentin, and β-catenin in vitro. Conclusion HOXD10 acts as a tumor suppressor and suppresses invasion and migration of CCRCC cells by regulating E-cadherin and EMT processes. Thus, targeting HOXD10 may be a therapeutic strategy for CCRCC treatment.


Pathology ◽  
2004 ◽  
Vol 36 (2) ◽  
pp. 145-151 ◽  
Author(s):  
Nives Pećina-Šlaus ◽  
Koraljka Gall-Trošelj ◽  
Mario Šlaus ◽  
Krešimir Radić ◽  
Tamara Nikuševa-Martić ◽  
...  

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Dingwei Xue ◽  
Huan Wang ◽  
Yuanlei Chen ◽  
Danyang Shen ◽  
Jieyang Lu ◽  
...  

Abstract Background Circular RNA (circRNA) is a type of circular endogenous RNA produced by special selective splicing and participates in progression of diverse diseases. However, the role of circRNA in clear cell renal cell carcinoma (ccRCC) is still rarely reported. Methods We detected lower circ-AKT3 expression in ccRCC using the circular RNA microarray. Then, qPCR array was applied to verify the expression of circ-AKT3 in between 60 ccRCC tissues and adjacent normal tissues, as well as ccRCC cell lines and human normal kidney cell (HK-2). We investigated the function of circ-AKT3 in ccRCC in vitro and in vivo and detected underlying mechanisms by Western blotting, bioinformatic analysis, RNA pull-down assay and luciferase reporter assay. Results Circ-AKT3 was verified significantly downregulated in ccRCC. Knockdown of circ-AKT3 promoted ccRCC migration and invasion, while overexpression of circ-AKT3 suppressed ccRCC metastasis. Further, circ-AKT3/miR-296-3p/E-cadherin axis was shown responsible for circ-AKT3 inhibiting ccRCC metastasis. Conclusion Circ-AKT3 suppresses ccRCC metastasis by enforcing E-cadherin expression through competitively binding miR-296-3p. Circ-AKT3 may therefore serve as a novel therapeutic to better suppress ccRCC metastasis.


2008 ◽  
Vol 88 (4) ◽  
pp. 450-450
Author(s):  
Michelle L Gervais ◽  
Pauline C Henry ◽  
Arthy Saravanan ◽  
T Nadine Burry ◽  
Brenda L Gallie ◽  
...  

2007 ◽  
Vol 177 (4S) ◽  
pp. 214-214
Author(s):  
Sung Kyu Hong ◽  
Byung Kyu Han ◽  
In Ho Chang ◽  
June Hyun Han ◽  
Ji Hyung Yu ◽  
...  

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