scholarly journals B7-H4 expression in renal cell carcinoma and tumor vasculature: Associations with cancer progression and survival

2006 ◽  
Vol 103 (27) ◽  
pp. 10391-10396 ◽  
Author(s):  
A. E. Krambeck ◽  
R. H. Thompson ◽  
H. Dong ◽  
C. M. Lohse ◽  
E. S. Park ◽  
...  
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.


2011 ◽  
Vol 58 (2) ◽  
pp. 191-197 ◽  
Author(s):  
Seong H Yoo ◽  
Kyoungbun Lee ◽  
Ji Y Chae ◽  
Kyung C Moon

2020 ◽  
Author(s):  
Bitian Liu ◽  
Xiaonan Chen ◽  
Yunhong Zhan ◽  
Bin Wu ◽  
Shen Pan

Abstract Background: Cancer-associated fibroblasts (CAFs) are most abundant in stroma and are critically involved in cancer progression. However, the specific signature of CAFs and related clinicopathological parameters in renal cell carcinoma (RCC) remain unclear. Methods: In this work, methods using recognized gene signatures were employed to roughly assess the infiltration level of the stroma and CAFs in RCC based on the data in The Cancer Genome Atlas. Weighted gene co-expression network analysis (WGCNA) was used to cluster transcriptomes and correlate with CAFs to identify specific markers. A comparison of fibroblast versus urothelial carcinoma cell lines and correlation with previously reported CAF markers were performed to demonstrate the specific expressed of the gene signature. The gene signature was used to compare fibroblast infiltration of each sample through single sample gene set enrichment analysis, and the clinical significance of fibroblasts was analyzed via Cox risk assessment and the chi-square test. Finally, we used validation data to verify the clinical significance of the fibroblast gene signature in RCC. Results: Roughly calculated tumor matrix and CAF levels were significantly higher in kidney cancer than in normal tissues. More than 85% of fibroblast-specific markers identified by WGCNA were consistent with markers obtained via single-cell sequencing. These markers were more highly expressed in fibroblast cell lines and were significantly correlated with canonical CAFs makers. Data validation also showed that CAFs were significant correlation with survival and pathological grade. Conclusions: In summary, our findings indicate that the gene signature potentially serves as a biomarker of CAFs in RCC and that infiltration of fibroblasts in RCC is an independent prognostic factor associated with pathological grade and stage of tumor. The ability to recognize specific CAF markers using WGCNA is comparable to single-cell sequencing.


2013 ◽  
Vol 49 (3) ◽  
pp. 320-328 ◽  
Author(s):  
E. V. Beresneva ◽  
S. V. Rykov ◽  
D. S. Khodyrev ◽  
I. V. Pronina ◽  
V. D. Ermilova ◽  
...  

2008 ◽  
Vol 14 (16) ◽  
pp. 5150-5157 ◽  
Author(s):  
Paul L. Crispen ◽  
Yuri Sheinin ◽  
Timothy J. Roth ◽  
Christine M. Lohse ◽  
Susan M. Kuntz ◽  
...  

2021 ◽  
Author(s):  
Ji Zhang ◽  
Shushu Yuan ◽  
Hua Zhu ◽  
Zhan Chen ◽  
Zhenmin Liu ◽  
...  

Abstract Background: Metastasis and drug resistance are the main causes of renal cell carcinoma (RCC) mortality. Currently, there are still limited number of targeted therapies against advanced RCC. It is critical to develop new effective clinical biomarkers and drug targets in RCC. Several studies have shown that Centromere protein F (CENPF), a microtubule binding protein, promotes cancer progression in various types of cancer. The purpose of this study is to explore the role of CENPF in RCC.Materials and methods: Peripheral blood and corresponding tissue samples of 23 RCC patients and 23 normal physical examination patients who were treated in our hospital from 2018 to 2020 were collected, and the CENPF expression was detected by qRT-PCR, Western-blot and immunohistochemical methods. Down-regulate the expression of CENPF by siRNA transfection, and detect the proliferation of the corresponding RCC cells and the corresponding cell cycle.Results: According to TCGA data analysis, CENPF is highly expressed in RCC, and its expression level is significantly related to the overall survival and recurrence-free survival of RCC. In addition, high expression of CENPF was found in the tissues of RCC patients in our hospital. Knockdown of CENPF can significantly reduce the proliferation of RCC cells in in vitro experiments, and knockdown of CENPF can regulate the cell cycle by inhibiting the expression of cyclins such as CDK4, CDK6 and CyclinD1. Conclusion: CENPF can be used as an independent prognostic factor of RCC and regulate the proliferation ability and cell cycle of RCC cells. CENPF is a potential oncogene and prognostic marker in RCC.


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