scholarly journals Fatty acid binding proteins (FABPs) in prostate, bladder and kidney cancer cell lines and the use of IL-FABP as survival predictor in patients with renal cell carcinoma

BMC Cancer ◽  
2011 ◽  
Vol 11 (1) ◽  
Author(s):  
Angelika Tölle ◽  
Saba Suhail ◽  
Monika Jung ◽  
Klaus Jung ◽  
Carsten Stephan
PROTEOMICS ◽  
2005 ◽  
Vol 5 (10) ◽  
pp. 2631-2640 ◽  
Author(s):  
Barbara Seliger ◽  
Rudolf Lichtenfels ◽  
Derek Atkins ◽  
Jürgen Bukur ◽  
Thomas Halder ◽  
...  

2022 ◽  
Vol 2022 ◽  
pp. 1-8
Author(s):  
Yunxiang Gong ◽  
Degang Wang ◽  
Wengang Wang

Objective. In this paper, we study the role of the VHL gene in regulating the proliferation and apoptosis of renal cell carcinoma, as well as the safety and transfection efficiency of ultrasound microbubble gene transfection technology. Method. We use kidney cancer cell lines as an in vitro research object and apply ultrasound microbubble gene transfection technology to transfect the VHL gene into kidney cancer cell line (786-0). The proliferation and apoptosis of cells were measured to clarify the inhibitory effect of the VHL gene in renal cell carcinoma. After that, pEGFP-VHL was transfected using ultrasonic microbubble and liposome gene transfection techniques, respectively, and the transfection efficiency was measured by immunofluorescence. Results. Compared with untreated and 786-0 cells that are transfected with empty vector, the expression level of VHL gene mRNA in 786-0 cells that are transfected with pcDNA3.1-VHL was significantly increased, and the cell growth inhibition rate was significantly higher. The rate of apoptosis increased significantly. Transfection efficiency of the pEGFP-VHL gene after transfection of 786-0 cells for 48 h: control group 0, liposome group ( 35.55 ± 2.77 ) %, ultrasound microbubble group ( 18.27 ± 2.83 ) %, and two transfection methods on cells. There is no significant difference in the impact of vitality. Conclusion. VHL gene expression can significantly inhibit the proliferation ability of renal cancer cell line 786-0 and promote its apoptosis. VHL gene is a potential target for gene therapy of kidney cancer.


Urology ◽  
2007 ◽  
Vol 69 (2) ◽  
pp. 236-240 ◽  
Author(s):  
Takumi Teratani ◽  
Tomohiro Domoto ◽  
Ken Kuriki ◽  
Teruyo Kageyama ◽  
Tatsuya Takayama ◽  
...  

2001 ◽  
Vol 16 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Robert O. Dillman ◽  
Neil M. Barth ◽  
Louis A. VanderMolen ◽  
David H. Garfield ◽  
Cristina De Leon ◽  
...  

Author(s):  
Youfeng Yang ◽  
Christopher J. Ricketts ◽  
Cathy D. Vocke ◽  
J. Keith Killian ◽  
Hesed M. Padilla‐Nash ◽  
...  

Genes ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 261 ◽  
Author(s):  
Patrick T. Gomella ◽  
W. Linehan ◽  
Mark W. Ball

Renal cell carcinoma is a term that represents multiple different disease processes, each driven by different genetic alterations, with distinct histology, and biological potential which necessitates divergent management strategies. This review discusses the genetic alterations seen in several forms of hereditary kidney cancer and how that knowledge can dictate when and how to intervene with a focus on the surgical management of these tumors.


Metabolites ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 1
Author(s):  
Tomonori Sato ◽  
Yoshihide Kawasaki ◽  
Masamitsu Maekawa ◽  
Shinya Takasaki ◽  
Kento Morozumi ◽  
...  

Metabolomics analysis possibly identifies new therapeutic targets in treatment resistance by measuring changes in metabolites accompanying cancer progression. We previously conducted a global metabolomics (G-Met) study of renal cell carcinoma (RCC) and identified metabolites that may be involved in sunitinib resistance in RCC. Here, we aimed to elucidate possible mechanisms of sunitinib resistance in RCC through intracellular metabolites. We established sunitinib-resistant and control RCC cell lines from tumor tissues of RCC cell (786-O)-injected mice. We also quantified characteristic metabolites identified in our G-Met study to compare intracellular metabolism between the two cell lines using liquid chromatography-mass spectrometry. The established sunitinib-resistant RCC cell line demonstrated significantly desuppressed protein kinase B (Akt) and mesenchymal-to-epithelial transition (MET) phosphorylation compared with the control RCC cell line under sunitinib exposure. Among identified metabolites, glutamine, glutamic acid, and α-KG (involved in glutamine uptake into the tricarboxylic acid (TCA) cycle for energy metabolism); fructose 6-phosphate, D-sedoheptulose 7-phosphate, and glucose 1-phosphate (involved in increased glycolysis and its intermediate metabolites); and glutathione and myoinositol (antioxidant effects) were significantly increased in the sunitinib-resistant RCC cell line. Particularly, glutamine transporter (SLC1A5) expression was significantly increased in sunitinib-resistant RCC cells compared with control cells. In this study, we demonstrated energy metabolism with glutamine uptake and glycolysis upregulation, as well as antioxidant activity, was also associated with sunitinib resistance in RCC cells.


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