Mechanism of Telomerase Reverse Transcriptase Regulating Dendritic Cell Immune Function in Proliferation and Cell Cycle of Renal Cell Carcinoma

2020 ◽  
Vol 10 (2) ◽  
pp. 195-202
Author(s):  
Yunxing Liu
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Flow Cytometry ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Renal Cancer ◽  
Renal Cell ◽  
Human Renal Cell Carcinoma ◽  
Renal Cancer Cell ◽  
Group A

To select human renal cell carcinoma cell lines VMRC-RCZ After resuscitation, culture and passage, the cell concentration was adjusted to 1 × 106/ml, and the experiment was divided into a control group, a renal cancer cell + DC group (DC group), and a renal cancer cell + DC+ hTERTtransfection group (transfection Group), a total of 3 groups; the recombinant eukaryotic expression plasmid hTERT-IRES2-EGFP was constructed and transfected into mature DC; the renal cancer cell + DC group was transfected with the empty plasmid, and the renal cancer cell + DC+ hTERT transfection group was transfected with the overexpression plasmid The transfection efficiency was detected by RT-PCR method. Cultured for 12 h and 24 h respectively, the percentage of HLA-DR, CD40 and MHC-II molecules in three groups of DC immunophenotypes was determined according to flow cytometry assay, and the cytokines IL-12 and TNF-α expression level, DC apoptosis rate was detected by in situ hybridization, the rate of tumor cell proliferation was measured according to MTT method, and cell cycle was determined through flow cytometry.

Induction of cell cycle arrest, DNA damage, and apoptosis by nimbolide in human renal cell carcinoma cells

Tumor Biology ◽  
2015 ◽  
Vol 36 (10) ◽  
pp. 7539-7547 ◽  
Author(s):  
Yi-Hsien Hsieh ◽  
Chien-Hsing Lee ◽  
Hsiao-Yun Chen ◽  
Shu-Ching Hsieh ◽  
Chia-Liang Lin ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Dna Damage ◽  
Cell Carcinoma ◽  
Cell Cycle Arrest ◽  
Renal Cell ◽  
Carcinoma Cells ◽  
Human Renal Cell Carcinoma ◽  
Cycle Arrest

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.

scholarly journals GATA3 suppresses human fibroblasts-induced metastasis of clear cell renal cell carcinoma via an anti-IL6/STAT3 mechanism

2019 ◽  
Vol 27 (9) ◽  
pp. 726-738 ◽  
Author(s):  
Qianqian Shi ◽  
Renfang Xu ◽  
Guanglai Song ◽  
Hao Lu ◽  
Dong Xue ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Cells ◽  
Conditioned Medium ◽  
Renal Cancer ◽  
Renal Cell ◽  
Clear Cell ◽  
Normal Fibroblast ◽  
Cell Renal Cell Carcinoma ◽  
Renal Cancer Cell

AbstractTumorigenesis and metastasis depend on intricate interactions between genetically altered tumor cells and their surrounding microenvironment. It is, however, unclear regarding the molecular mechanisms underlying the progress and metastasis of human clear-cell renal cell carcinoma in the microenvironment with fibroblasts. In this work, we investigated the effect of normal fibroblasts on the metastasis of renal cancer and the relevant signaling pathways. We isolated normal fibroblasts from normal renal tissues and used normal fibroblast-conditioned medium culture renal cancer cells. The CCK-8 and transwell assays showed that normal fibroblasts conditioned medium significantly enhanced ccRCC cell migration. IL6 mediated the cross talk between normal fibroblasts and the cancer cells, and promoted tumor cell migration through the STAT3 pathway. In contrast, GATA3 was downregulated at both mRNA and protein levels in the normal fibroblast-conditioned medium treated with renal cancer cells, but upregulated in adjacent normal tissues. GATA3 overexpression significantly reduced STAT3 phosphorylation and attenuated the migration in both renal cancer cell and IL6-stimulated renal cancer cell. Taken together, our findings suggest that the IL6/STAT3 pathway plays a crucial role in the normal fibroblast-enhanced clear-cell renal cell carcinoma metastasis, while GATA3 may mitigate this effect by inhibiting IL6/STAT3 signaling.

scholarly journals Tanshinone IIA arrests cell cycle and induces apoptosis in 786-O human renal cell carcinoma cells

2012 ◽  
Vol 3 (5) ◽  
pp. 1144-1148 ◽  
Author(s):  
XIANLI WEI ◽  
LUNBIN ZHOU ◽  
LIANGYONG HU ◽  
YAOXIONG HUANG
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Carcinoma Cells ◽  
Tanshinone Iia ◽  
Human Renal Cell Carcinoma

Downregulation of ABCD1 in Human Renal Cell Carcinoma

2009 ◽  
Vol 24 (3) ◽  
pp. 171-178 ◽  
Author(s):  
Tzyh-Chyuan Hour ◽  
Yi-Zih Kuo ◽  
Guang-Yaw Liu ◽  
Wang-Yi Kang ◽  
Chao-Yuan Huang ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Delayed Diagnosis ◽  
Human Renal Cell Carcinoma ◽  
Renal Tubular Cells ◽  
Renal Cancer Cell ◽  
Tumor Stages ◽  
Mrna And Protein Expression ◽  
Renal Tubular

Renal cell carcinoma (RCC) is the most common malignant tumor of the kidney. Delayed diagnosis may result in progression and metastasis. Markers for early detection of RCC are lacking. The ATP-binding cassette transporter D1 (ABCD1) is located in the human peroxisome membrane. Its mutation causes X-linked adrenoleukodystrophy (X-ALD), a peroxisomal disorder affecting lipid storage. The role of ABCD1 in human renal tumorigenesis was unclear. In this study, three pairs of RCC tissues were examined by cDNA microarray and data suggested that ABCD1 mRNA is downregulated. Downregulation of ABCD1 expression was confirmed by real-time PCR. ABCD1 expression was also downregulated in four renal cancer cell lines compared to immortalized benign renal tubular cells. ABCD1 mRNA and protein expression levels assessed by immunohistochemistry in the RCC tissues were similar between genders, tumor grades, and tumor stages. Immunohisto-chemical assays also showed that ABCD1 expression was significantly higher in normal than in cancerous tissues (p<0.001). ABCD1 downregulation may be involved in human renal tumorigenesis.

scholarly journals Circ_RPL23A acts as a miR-1233 sponge to suppress the progression of clear cell renal cell carcinoma by promoting ACAT2

2020 ◽  
Author(s):  
Liang Cheng ◽  
Huifeng Cao ◽  
Jianbo Xu ◽  
Mo Xu ◽  
Wenjie He ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Flow Cytometry ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Clear Cell ◽  
Xenograft Model ◽  
Luciferase Reporter ◽  
Cell Renal Cell Carcinoma ◽  
Mesenchymal Transition

Abstract Background Clear cell renal cell carcinoma (CCRCC) is a prevalent urological carcinoma with high metastatic risk. Circular RNAs (circRNAs) have been identified as effective diagnostic and therapeutic biomarkers for CCRCC. This research aims to disclose the involvement of circRNA ribosomal protein L23a (circ_RPL23A) in CCRCC, and how it regulates carcinogenesis. Methods We performed quantitative real-time polymerase chain reaction (qRT-PCR) to examine circ_RPL23A, microRNA-1233 (miR-1233) and acetyl-coenzyme A acetyltransferase 2 (ACAT2). Cellular behavior detection included cell cycle, proliferation, apoptosis and metastasis, which were severally analyzed using propidium iodide (PI)-flow cytometry, 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT), Annexin V/PI-flow cytometry and transwell migration/invasion assays. ACAT2 and related proteins of cell cycle, epithelial-mesenchymal transition (EMT) were measured via western blot. Target relationship was analyzed via dual-luciferase reporter assay. A xenograft model was used to study circ_RPL23A action in mice. Results Both in CCRCC tissues and cells, circ_RPL23A had a down-regulated tendency. Explicitly, circ_RPL23A overexpression inhibited cell cycle, proliferation and metastasis but enhanced apoptosis of CCRCC cells, whereas these effects of circ_RPL23A were dependent on the suppression of its target miR-1233. Besides, miR-1233 could target ACAT2 and circ_RPL23A regulated ACAT2 by sponging miR-1233. Also importantly, miR-1233 was a pro-cancer gene in CCRCC via targeting ACAT2. CCRCC tumor growth was also decreased in vivo by circ_RPL23A through miR-1233/ACAT2 axis. Conclusion Altogether, the circ_RPL23A/miR-1233/ACAT2 axis in this report provides an in-depth cognition for CCRCC pathogenesis and circ_RPL23A may has pivotal value in diagnosing and treating CCRCC.

scholarly journals Expression and regulatory effects on cancer cell behavior of NELL1 and NELL2 in human renal cell carcinoma

2015 ◽  
Vol 106 (5) ◽  
pp. 656-664 ◽  
Author(s):  
Ritsuko Nakamura ◽  
Takeru Oyama ◽  
Ryosuke Tajiri ◽  
Atsushi Mizokami ◽  
Mikio Namiki ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Renal Cell ◽  
Cell Behavior ◽  
Human Renal Cell Carcinoma ◽  
Regulatory Effects

scholarly journals Circ_RPL23A acts as a miR-1233 sponge to suppress the progression of clear cell renal cell carcinoma by promoting ACAT2

2020 ◽  
Author(s):  
Liang Cheng ◽  
Huifeng Cao ◽  
Jianbo Xu ◽  
Mo Xu ◽  
Wenjie He ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Flow Cytometry ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Clear Cell ◽  
Xenograft Model ◽  
Luciferase Reporter ◽  
Cell Renal Cell Carcinoma ◽  
Mesenchymal Transition

Abstract Background Clear cell renal cell carcinoma (CCRCC) is a prevalent urological carcinoma with high metastatic risk. Circular RNAs (circRNAs) have been identified as effective diagnostic and therapeutic biomarkers for CCRCC. This research aims to disclose the involvement of circRNA ribosomal protein L23a (circ_RPL23A) in CCRCC, and how it regulates carcinogenesis. Methods We performed quantitative real-time polymerase chain reaction (qRT-PCR) to examine circ_RPL23A, microRNA-1233 (miR-1233) and acetyl-coenzyme A acetyltransferase 2 (ACAT2). Cellular behavior detection included cell cycle, proliferation, apoptosis and metastasis, which were severally analyzed using propidium iodide (PI)-flow cytometry, 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT), Annexin V/PI-flow cytometry and transwell migration/invasion assays. ACAT2 and related proteins of cell cycle, epithelial-mesenchymal transition (EMT) were measured via western blot. Target relationship was analyzed via dual-luciferase reporter assay. A xenograft model was used to study circ_RPL23A action in mice. Results Both in CCRCC tissues and cells, circ_RPL23A had a down-regulated tendency. Explicitly, circ_RPL23A overexpression inhibited cell cycle, proliferation and metastasis but enhanced apoptosis of CCRCC cells, whereas these effects of circ_RPL23A were dependent on the suppression of its target miR-1233. Besides, miR-1233 could target ACAT2 and circ_RPL23A regulated ACAT2 by sponging miR-1233. Also importantly, miR-1233 was a pro-cancer gene in CCRCC via targeting ACAT2. CCRCC tumor growth was also decreased in vivo by circ_RPL23A through miR-1233/ACAT2 axis. Conclusion Altogether, the circ_RPL23A/miR-1233/ACAT2 axis in this report provides an in-depth cognition for CCRCC pathogenesis and circ_RPL23A may has pivotal value in diagnosing and treating CCRCC.

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