scholarly journals The effect of Aurora kinases on cell proliferation, cell cycle regulation and metastasis in renal cell carcinoma

2012 ◽  
Vol 41 (6) ◽  
pp. 2139-2149 ◽  
Author(s):  
YAN LI ◽  
WANQI ZHOU ◽  
LANGLI WEI ◽  
JING JIN ◽  
KE TANG ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Cell Cycle Regulation ◽  
Aurora Kinases ◽  
Cycle Regulation

scholarly journals JAK3/STAT5/6 Pathway Alterations Are Associated with Immune Deviation inCD8+T Cells in Renal Cell Carcinoma Patients

2010 ◽  
Vol 2010 ◽  
pp. 1-13 ◽  
Author(s):  
Elisabetta Cavalcanti ◽  
Margherita Gigante ◽  
Vito Mancini ◽  
Michele Battaglia ◽  
Pasquale Ditonno ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
T Cells ◽  
T Cell ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Cell Cycle Regulation ◽  
T Cell Response ◽  
T Cell Subsets ◽  
Cycle Regulation

To investigate the molecular mechanisms underlying altered T cell response in renal cell carcinoma (RCC) patients, we compared autologous and allogeneicCD8+T cell responses against RCC line from RCC patients and their HLA-matched donors, using mixed lymphocyte/tumor cell cultures (MLTCs). In addition, we analyzed the expression of molecules associated with cell cycle regulation. Autologous MLTC responderCD8+T cells showed cytotoxic activity against RCC cell lines; however the analysis of the distribution ofCD8+T-cell subsets revealed that allogenic counterparts mediate superior antitumor efficacy. In RCC patients, a decreased proliferative response to tumor, associated with defects in JAK3/STAT5/6 expression that led to increased p27KIP1 expression and alterations in the cell cycle, was observed. These data define a molecular pathway involved in cell cycle regulation that is associated with the dysfunction of tumor-specificCD8+effector cells. If validated, this may define a therapeutic target in the setting of patients with RCC.

scholarly journals miR-129-5p inhibits clear cell renal cell carcinoma cell proliferation, migration and invasion by targeting SPN

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Bin Gao ◽  
Lijuan Wang ◽  
Na Zhang ◽  
Miaomiao Han ◽  
Yubo Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Clear Cell ◽  
Luciferase Assay ◽  
Cell Renal Cell Carcinoma ◽  
Regulated Expression ◽  
Ccrcc Cell

Abstract Objective Our study aims to investigate the mechanism of the miR-129-5p/SPN axis in clear cell renal cell carcinoma (ccRCC), providing a novel direction for the targeted therapy of ccRCC. Methods Bioinformatics methods were implemented to find the differentially expressed genes (DEGs) associated with ccRCC from TCGA database. qRT-PCR was performed to detect miR-129-5p and SPN mRNA expression, while western bot was carried out for the detection of protein expression of SPN. Bioinformatics analysis was used to predict the binding sites of miR-129-5p on SPN 3’UTR, while dual-luciferase assay was conducted to verify their binding relationship. CCK-8 assay, colony formation assay, wound healing assay and Transwell assay were employed to measure ccRCC cell proliferative ability, cell formation ability, cell migratory and invasive abilities. Flow cytometry was implemented to assess cell cycle and apoptosis. Results miR-129-5p exhibited a significantly down-regulated expression level in ccRCC, while SPN showed a remarkably up-regulated expression level. Overexpressed miR-129-5p inhibited ccRCC cell proliferative, invasive and migratory capacities while induced cell cycle arrest in G0/G1 phase and promoted cell apoptosis. Dual-luciferase assay confirmed that there was a binding relationship between miR-129-5p and SPN. Moreover, overexpressed miR-129-5p remarkably reduced SPN expression in cancer cells, weakened the promoting effect of SPN on cell proliferation, migration, invasion and cell cycle progress, and led to enhanced cell apoptotic activity. Conclusions Our study proves the regulatory effect of the miR-129-5p/SPN axis in ccRCC, and provides a novel potential target for precise treatment of patients with ccRCC.

scholarly journals miR-129-5p inhibits clear cell renal cell carcinoma cell proliferation, migration and invasion by targeting SPN

2021 ◽  
Author(s):  
Bin Gao ◽  
Lijuan Wang ◽  
Yubo Zhang ◽  
Na Zhang ◽  
Miaomiao Han ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Clear Cell ◽  
Luciferase Assay ◽  
Cell Renal Cell Carcinoma ◽  
Regulated Expression ◽  
Ccrcc Cell

Abstract Objective: Our study aims to investigate the mechanism of the miR-129-5p/SPN axis in clear cell renal cell carcinoma (ccRCC), providing a novel direction for the targeted therapy of ccRCC. Methods: Bioinformatics methods were implemented to find the differentially expressed genes (DEGs) associated with ccRCC from TCGA database. qRT-PCR was performed to detect miR-129-5p and SPN mRNA expression, while western bot was carried out for the detection of protein expression of SPN. Bioinformatics analysis was used to predict the binding sites of miR-129-5p on SPN 3’UTR, while dual-luciferase assay was conducted to verify their binding relationship. CCK-8 assay, colony formation assay, wound healing assay and Transwell assay were employed to measure ccRCC cell proliferative ability, cell formation ability, cell migratory and invasive abilities. Flow cytometry was implemented to assess cell cycle and apoptosis. Results: miR-129-5p exhibited a significantly down-regulated expression level in ccRCC, while SPN showed a remarkably up-regulated expression level. Overexpressed miR-129-5p inhibited ccRCC cell proliferative, invasive and migratory capacities while induced cell cycle arrest in G0/G1 phase and promoted cell apoptosis. Dual-luciferase assay confirmed that there was a binding relationship between miR-129-5p and SPN. Moreover, overexpressed miR-129-5p remarkably reduced SPN expression in cancer cells, weakened the promoting effect of SPN on cell proliferation, migration, invasion and cell cycle progress, and led to enhanced cell apoptotic activity.Conclusion: Our study proves the regulatory effect of the miR-129-5p/SPN axis in ccRCC, and provides a novel potential target for precise treatment of patients with ccRCC.

scholarly journals Nobiletin Down-regulates SKP2-p21/p27-CDK2 Axis to Inhibit Tumor Progression and Shows Synergistic Effect with Palbociclib on Renal Cell Carcinoma

2020 ◽  
Author(s):  
Tingting Chen ◽  
Liu Liu ◽  
Xiaoyan Hu ◽  
Kai Wang ◽  
Tao Zhou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Tumor Formation ◽  
Phase Cell ◽  
Pcr Analysis ◽  
Nude Mouse Model

Abstract Background: Natural extracts can enhance the efficacy and sensitivity of chemotherapeutic drugs, including nobiletin. However, the possible role and underlying mechanisms of nobiletin in cancer including Renal cell carcinoma (RCC) are still unclear.Methods：Cell proliferation, cell cycle and apoptosis analysis, colony-forming assays, immunoblotting analysis and qRT-PCR analysis were performed to investigate how nobiletin inhibits RCC cell proliferation in vitro. Nude mouse model was used to measure in vivo efficacy of nobiletin and its combination with palbociclib.Results：Nobiletin induced G1 phase cell cycle arrest, apoptosis, and proliferative inhibition in RCC Cells. Mechanistically, nobiletin inhibited activation of oncogene SKP2, leading to the accumulation of tumor suppressors and apoptosis-inducing substrates such as p21 and p27 to inhibit cell proliferation, eventually inhibit tumor formation. Intriguingly, we further found that sensitivity of palbociclib was associated with SKP2 protein level. Furthermore, in vitro and vivo results, dual inhibition of nobiletin and palbociclib showed synergistic lethality.Conclusion：Combination nobiletin and palbociclib may serve as a potential therapeutic strategy for renal cancer.

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