Elevated in vitro translation of a 25-kDa protein in renal cell carcinoma

1991 ◽  
Vol 69 (8) ◽  
pp. 561-565 ◽  
Author(s):  
Gilles Paradis ◽  
Josée Gaudreau ◽  
Gilles Frenette ◽  
Michel Thabet ◽  
Roland R. Tremblay ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Normal Tissue ◽  
Sodium Dodecyl ◽  
In Vitro Translation ◽  
Translation Product ◽  
Primary Translation Product ◽  
Rabbit Reticulocyte Lysate System

As a first step in understanding the changes in protein synthesis that occur in renal cell carcinoma, we have prepared poly(A)+ RNA from surgically removed tumors and from their normal tissue counterpart. These RNAs were then translated in vitro in the rabbit reticulocyte lysate system and the synthesized labeled polypeptides were separated by one- and two-dimensional gel electrophoresis. A major 25-kDa primary translation product was observed with all renal cell carcinomas. The synthesis of this protein was barely detectable with the RNA from normal tissue adjacent to the tumor. To determine if this protein could be further processed (removal of signal peptide and (or) core glycosylation), canine pancreatic microsomal membranes were added to the system. This addition resulted in the formation of a vertical row of three additional spots, with the same isoelectric point as the primary translation product and with molecular masses ranging from 27 to 31 kDa. The 31-kDa protein was retained on Concanavalin A. After digestion with endoglycosidase H, it was no longer visible on sodium dodecyl sulfate gels and a new 27-kDa band was generated suggesting that the mature protein was indeed a glycoprotein. Future experiments will be aimed at identifying this protein and examining its potential value as a marker of renal cell carcinoma.Key words: renal cancer, post-translational modifications, glycosylation, tumor markers.

MicroRNA-21 is Overexpressed in Renal Cell Carcinoma

2013 ◽  
Vol 28 (2) ◽  
pp. 201-207 ◽  
Author(s):  
Lu Lv ◽  
Fengxian Huang ◽  
Haiping Mao ◽  
Ming Li ◽  
Xiaoyan Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Normal Tissue ◽  
Cell Cycle Progression ◽  
Expression Profiles ◽  
Adjacent Normal Tissue ◽  
Rt Pcr

Objective To identify microRNAs (miRNAs) that are overexpressed in renal cell carcinoma (RCC) and characterize the functional role of miR-21. Materials and Methods The miRNA expression profiles between RCC tissue and adjacent normal tissue were compared using microarray analysis. The differential expression of miR-21 was validated by real-time polymerase chain reaction (RT-PCR). 786-O RCC cells were transfected with miR-21 mimic, miR-21 inhibitor, or negative controls and cell proliferation, apoptosis and cell cycle were examined by MTT assay and flow cytometry. The expression of programmed cell death 4 (PDCD4) and tropomyosin 1 (TPM1) was detected by RT-PCR and Western blot analysis. Results Compared to adjacent normal tissue, 10 human miRNAs were significantly upregulated and 7 were downregulated in RCC tissue. RT-PCR confirmed that miR-21 was significantly overexpressed in RCC tissue. In vitro expression of miR-21 mimic promoted the growth of 786-O cells, whereas miR-21 inhibitor inhibited cell growth by inducing apoptosis and cell cycle arrest at S phase. Furthermore, miR-21 mimic or inhibitor significantly reduced or increased the expression of PDCD4 and TPM1. Conclusions MiR-21 is overexpressed in RCC tissue and modulates the growth, apoptosis and cell cycle progression of RCC cells and regulates the expression of PDCD4 and TPM1.

scholarly journals Clinicopathologic features of TDO2 overexpression in renal cell carcinoma

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Quoc Thang Pham ◽  
Daiki Taniyama ◽  
Yohei Sekino ◽  
Shintaro Akabane ◽  
Takashi Babasaki ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
In Silico Analysis ◽  
Immunohistochemical Analysis ◽  
Rna Seq ◽  
Anoikis Resistance ◽  
Silico Analysis ◽  
Proliferation And Invasion

Abstract Background Tryptophan 2,3-dioxygenase (TDO2) is the primary enzyme catabolizing tryptophan. Several lines of evidence revealed that overexpression of TDO2 is involved in anoikis resistance, spheroid formation, proliferation, and invasion and correlates with poor prognosis in some cancers. The aim of this research was to uncover the expression and biofunction of TDO2 in renal cell carcinoma (RCC). Methods To show the expression of TDO2 in RCC, we performed qRT-PCR and immunohistochemistry in integration with TCGA data analysis. The interaction of TDO2 with PD-L1, CD44, PTEN, and TDO2 expression was evaluated. We explored proliferation, colony formation, and invasion in RCC cells line affected by knockdown of TDO2. Results RNA-Seq and immunohistochemical analysis showed that TDO2 expression was upregulated in RCC tissues and was associated with advanced disease and poor survival of RCC patients. Furthermore, TDO2 was co-expressed with PD-L1 and CD44. In silico analysis and in vitro knockout of PTEN in RCC cell lines revealed the ability of PTEN to regulate the expression of TDO2. Knockdown of TDO2 suppressed the proliferation and invasion of RCC cells. Conclusion Our results suggest that TDO2 might have an important role in disease progression and could be a promising marker for targeted therapy in RCC. (199 words)

scholarly journals Circular RNA circSDHC serves as a sponge for miR-127-3p to promote the proliferation and metastasis of renal cell carcinoma via the CDKN3/E2F1 axis

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Junjie Cen ◽  
Yanping Liang ◽  
Yong Huang ◽  
Yihui Pan ◽  
Guannan Shu ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Target Genes ◽  
Expression Patterns ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Proliferation And Metastasis

Abstract Background There is increasing evidence that circular RNAs (circRNAs) have significant regulatory roles in cancer development and progression; however, the expression patterns and biological functions of circRNAs in renal cell carcinoma (RCC) remain largely elusive. Method Bioinformatics methods were applied to screen for circRNAs differentially expressed in RCC. Analysis of online circRNAs microarray datasets and our own patient cohort indicated that circSDHC (hsa_circ_0015004) had a potential oncogenic role in RCC. Subsequently, circSDHC expression was measured in RCC tissues and cell lines by qPCR assay, and the prognostic value of circSDHC evaluated. Further, a series of functional in vitro and in vivo experiments were conducted to assess the effects of circSDHC on RCC proliferation and metastasis. RNA pull-down assay, luciferase reporter and fluorescent in situ hybridization assays were used to confirm the interactions between circSDHC, miR-127-3p and its target genes. Results Clinically, high circSDHC expression was correlated with advanced TNM stage and poor survival in patients with RCC. Further, circSDHC promoted tumor cell proliferation and invasion, both in vivo and in vitro. Analysis of the mechanism underlying the effects of circSDHC in RCC demonstrated that it binds competitively to miR-127-3p and prevents its suppression of a downstream gene, CDKN3, and the E2F1 pathway, thereby leading to RCC malignant progression. Furthermore, knockdown of circSDHC caused decreased CDKN3 expression and E2F1 pathway inhibition, which could be rescued by treatment with an miR-127-3p inhibitor. Conclusion Our data indicates, for the first time, an essential role for the circSDHC/miR-127-3p/CDKN3/E2F1 axis in RCC progression. Thus, circSDHC has potential to be a new therapeutic target in patients with RCC.

scholarly journals Neuropilin 1 and Neuropilin 2 gene invalidation or pharmacological inhibition reveals their relevance for the treatment of metastatic renal cell carcinoma

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Aurore Dumond ◽  
Etienne Brachet ◽  
Jérôme Durivault ◽  
Valérie Vial ◽  
Anna K. Puszko ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Cell Metabolism ◽  
Boyden Chamber ◽  
Migration Ability ◽  
Cell Renal Cell Carcinoma ◽  
Immunodeficient Mice ◽  
And Migration

Abstract Background Despite the improvement of relapse-free survival mediated by anti-angiogenic drugs like sunitinib (Sutent®), or by combinations of anti-angiogenic drugs with immunotherapy, metastatic clear cell Renal Cell Carcinoma (mccRCC) remain incurable. Hence, new relevant treatments are urgently needed. The VEGFs coreceptors, Neuropilins 1, 2 (NRP1, 2) are expressed on several tumor cells including ccRCC. We analyzed the role of the VEGFs/NRPs signaling in ccRCC aggressiveness and evaluated the relevance to target this pathway. Methods We correlated the NRP1, 2 levels to patients’ survival using online available data base. Human and mouse ccRCC cells were knocked-out for the NRP1 and NRP2 genes by a CRISPR/Cas9 method. The number of metabolically active cells was evaluated by XTT assays. Migration ability was determined by wound closure experiments and invasion ability by using Boyden chamber coated with collagen. Production of VEGFA and VEGFC was evaluated by ELISA. Experimental ccRCC were generated in immuno-competent/deficient mice. The effects of a competitive inhibitor of NRP1, 2, NRPa-308, was tested in vitro and in vivo with the above-mentioned tests and on experimental ccRCC. NRPa-308 docking was performed on both NRPs. Results Knock-out of the NRP1 and NRP2 genes inhibited cell metabolism and migration and stimulated the expression of VEGFA or VEGFC, respectively. NRPa-308 presented a higher affinity for NRP2 than for NRP1. It decreased cell metabolism and migration/invasion more efficiently than sunitinib and the commercially available NRP inhibitor EG00229. NRPa-308 presented a robust inhibition of experimental ccRCC growth in immunocompetent and immunodeficient mice. Such inhibition was associated with decreased expression of several pro-tumoral factors. Analysis of the TCGA database showed that the NRP2 pathway, more than the NRP1 pathway correlates with tumor aggressiveness only in metastatic patients. Conclusions Our study strongly suggests that inhibiting NRPs is a relevant treatment for mccRCC patients in therapeutic impasses and NRPa-308 represents a relevant hit.

Malignant phenotype of renal cell carcinoma cells is switched by Ukrain administration in vitro

2011 ◽  
Vol 22 (8) ◽  
pp. 749-762 ◽  
Author(s):  
Nicoletta Gagliano ◽  
Letizia Pettinari ◽  
Massimo Aureli ◽  
Carla Martinelli ◽  
Elena Colombo ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Carcinoma Cells ◽  
Malignant Phenotype

scholarly journals COP1 is downregulated in renal cell carcinoma (RCC) and inhibits the migration of RCC ACHN cells in vitro

2016 ◽  
Vol 14 (2) ◽  
pp. 1371-1378 ◽  
Author(s):  
La Ta ◽  
Chengrui Xuan ◽  
Nianzeng Xing ◽  
Xiaojun Zhu
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell

scholarly journals MicroRNA-373 promotes tumorigenesis of renal cell carcinoma in vitro and in vivo

2017 ◽  
Vol 16 (5) ◽  
pp. 7048-7055 ◽  
Author(s):  
Yanli Li ◽  
Da Zhang ◽  
Jiaxiang Wang
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell

Pro-apoptotic effects of Amblyomin-X in murine renal cell carcinoma “in vitro”

2012 ◽  
Vol 66 (1) ◽  
pp. 64-69 ◽  
Author(s):  
Erica Mie Akagi ◽  
Paulo Luiz de Sá Júnior ◽  
Simone Michaela Simons ◽  
Maria Helena Bellini ◽  
Sandra Alves Barreto ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Apoptotic Effects
Sign in / Sign up

Export Citation Format

Share Document