scholarly journals ARHGAP24 inhibits cell cycle progression, induces apoptosis and suppresses invasion in renal cell carcinoma

Oncotarget ◽  
2016 ◽  
Vol 7 (32) ◽  
pp. 51829-51839 ◽  
Author(s):  
Gaosi Xu ◽  
Xiongbing Lu ◽  
Tianlun Huang ◽  
Jie Fan
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Cell Cycle Progression ◽  
Cycle Progression

scholarly journals Cell cycle progression score predicts metastatic progression of clear cell renal cell carcinoma after resection

2015 ◽  
Vol 15 (6) ◽  
pp. 861-867 ◽  
Author(s):  
Eric J. Askeland ◽  
Vincent A. Chehval ◽  
Ryan W. Askeland ◽  
Placede G. Fosso ◽  
Zaina Sangale ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Cell Cycle Progression ◽  
Clear Cell ◽  
Metastatic Progression ◽  
Cell Renal Cell Carcinoma ◽  
Cycle Progression

scholarly journals Molecular and Functional Analysis of Sunitinib-Resistance Induction in Human Renal Cell Carcinoma Cells

2021 ◽  
Vol 22 (12) ◽  
pp. 6467
Author(s):  
Magdalena Rausch ◽  
Adriano Rutz ◽  
Pierre-Marie Allard ◽  
Céline Delucinge-Vivier ◽  
Mylène Docquier ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Cell Cycle Progression ◽  
Mass Spectrometry Analysis ◽  
Cycle Progression ◽  
Human Renal Cell Carcinoma ◽  
Resistance Induction ◽  
Extracellular Matrix Components

Resistance in clear cell renal cell carcinoma (ccRCC) against sunitinib is a multifaceted process encompassing numerous molecular aberrations. This induces clinical complications, reducing the treatment success. Understanding these aberrations helps us to select an adapted treatment strategy that surpasses resistance mechanisms, reverting the treatment insensitivity. In this regard, we investigated the dominant mechanisms of resistance to sunitinib and validated an optimized multidrug combination to overcome this resistance. Human ccRCC cells were exposed to single or chronic treatment with sunitinib to obtain three resistant clones. Upon manifestation of sunitinib resistance, morphometric changes in the cells were observed. At the molecular level, the production of cell membrane and extracellular matrix components, chemotaxis, and cell cycle progression were dysregulated. Molecules enforcing the cell cycle progression, i.e., cyclin A, B1, and E, were upregulated. Mass spectrometry analysis revealed the intra- and extracellular presence of N-desethyl sunitinib, the active metabolite. Lysosomal sequestration of sunitinib was confirmed. After treatment with a synergistic optimized drug combination, the cell metabolic activity in Caki-1-sunitinib-resistant cells and 3D heterotypic co-cultures was reduced by >80%, remaining inactive in non-cancerous cells. These results demonstrate geno- and phenotypic changes in response to sunitinib treatment upon resistance induction. Mimicking resistance in the laboratory served as a platform to study drug responses.

The Cell Cycle Progression Score: Unclear Role in Renal Cell Carcinoma

2018 ◽  
Vol 74 (1) ◽  
pp. 128-129 ◽  
Author(s):  
Daiki Ueno ◽  
Garrett M. Dancik ◽  
Brian Shuch
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Cell Cycle Progression ◽  
Cycle Progression

scholarly journals The role of CRP and ATG9B expression in clear cell renal cell carcinoma

2017 ◽  
Vol 37 (6) ◽  
Author(s):  
Zheng Ma ◽  
Zengguang Qi ◽  
Zhengfei Shan ◽  
Jiangsong Li ◽  
Jing Yang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Distant Metastasis ◽  
Renal Cell ◽  
Cell Cycle Progression ◽  
Clear Cell ◽  
Cell Renal Cell Carcinoma ◽  
Cycle Progression ◽  
Ccrcc Cell

The purpose of the study is to investigate the correlation between the expression of C-reactive protein (CRP) and autophagy-related 9B (ATG9B) and pathological features of clear cell renal cell carcinoma (CCRCC) patients. We also intended to explore the effects of manipulated expression of CRP and ATG9B on the apoptosis and cell cycle progression of CCRCC cell line. ATG9B expression in CCRCC tissues and adjacent renal tissues was analyzed by immunohistochemistry (IHC). Gene expression was determined at transcription and translational levels using real-time quantitative PCR (RT-qPCR) and Western blot. The association between CRP/ATG9B expression and clinical-pathological parameters including age, gender, pathological grades, TNM stage and distant metastasis of the patients was assessed by correlation analysis. siRNA and overexpression plasmids construction were used to manipulate the expression of CRP in human CCRCC cell line 786-O. Cell apoptosis and cell cycle progression were determined using flow cytometry (FCM) and Hoechst 33258 staining. CRP expression correlates with ATG9B expression. The expression of CRP and ATG9B are significantly correlated with TNM staging, distant metastasis, and survival time of CCRCC patients. A high-level of CRP indicates a poor overall survival (OS). In addition, CRP expression influences cell cycle and apoptosis of CCRCC cells. The study reveals that CRP might be a CCRCC development promoter. In addition, there is a close relationship between CRP and ATG9B in CCRCC carcinogenesis.

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.

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