MiR-193a-3p and miR-224 mediate renal cell carcinoma progression by targeting alpha-2,3-sialyltransferase IV and the phosphatidylinositol 3 kinase/Akt pathway

2018 ◽  
Vol 57 (8) ◽  
pp. 1067-1077 ◽  
Author(s):  
Yue Pan ◽  
Jialei Hu ◽  
Jia Ma ◽  
Xia Qi ◽  
Huimin Zhou ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Akt Pathway ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

scholarly journals The PI3K/AKT Pathway and Renal Cell Carcinoma

2015 ◽  
Vol 42 (7) ◽  
pp. 343-353 ◽  
Author(s):  
Huifang Guo ◽  
Peter German ◽  
Shanshan Bai ◽  
Sean Barnes ◽  
Wei Guo ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Akt Pathway

scholarly journals Cytotoxicity of 15-Deoxy-Δ12,14-prostaglandin J2 through PPARγ-independent Pathway and the Involvement of the JNK and Akt Pathway in Renal Cell Carcinoma

2012 ◽  
Vol 9 (7) ◽  
pp. 555-566 ◽  
Author(s):  
Megumi Fujita ◽  
Chiaki Tohji ◽  
Yoko Honda ◽  
Yasuhiro Yamamoto ◽  
Tsutomu Nakamura ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Akt Pathway ◽  
Prostaglandin J2

Long Noncoding RNA LINC00460 Facilitates the Proliferation and Metastasis of Renal Cell Carcinoma via PI3K/AKT Signaling Pathway

2021 ◽  
Author(s):  
Feng-Juan Zhou ◽  
Sen Meng ◽  
Hongmei Yong ◽  
Ping-Fu Hou ◽  
Min-Le Li ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Renal Cell ◽  
Noncoding Rna ◽  
Underlying Mechanism ◽  
The Cancer Genome Atlas ◽  
Akt Pathway

Abstract Renal cell carcinoma (RCC) is one of the most prevalent cancers. Long noncoding RNAs (LncRNAs) have been indicated as a mediator acted in tumorigenesis of RCC. However, the mechanism of LINC00460 on RCC is yet to be investigated. This study aimed to investigate the potential function of LINC00460 and underlying mechanism of RCC. We detected LINC00460 expression in RCC tissues and the prognosis in RCC patients using Gene Expression Profiling Interactive Analysis (GEPIA) website and The Cancer Genome Atlas (TCGA) database. LINC00460 level in normal renal cell line and RCC cell lines were detected by quantitative real-time polymerase chain reaction (qRT-PCR). We study the effects of LINC00460 on proliferation, migration, invasion, apoptosis in RCC cells lines using a series of in vivo and in vitro experiments. RNA sequencing (RNA-seq) analysis for the whole transcriptome was applied to searching potential LINC00460 related signal pathway in RCC. We identified the significant up-regulated expression level of LINC00460 in RCC tissues and cell lines. Elevated LINC00460 was correlated with shorter survival of RCC patients. Overexpression of LINC00460 promoted cell viability, proliferation, invasion and migration, while down-regulation of LINC00460 exerted inhibitory effect on these activities. We crucially identified that LNC00460 promotes development of RCC by influencing the PI3K/AKT pathway. Knockdown of LNC00460 decreased the phosphorylation of AKT and mTOR. The key finding of our study provided a new evidence suggesting that LINC00460 functions as an oncogene in RCC pathogenesis by mediating the PI3K/AKT pathway, which may provide a new target for the treatment of RCC.

scholarly journals Progress of Molecular Targeted Therapies for Advanced Renal Cell Carcinoma

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Alessandro Conti ◽  
Matteo Santoni ◽  
Consuelo Amantini ◽  
Luciano Burattini ◽  
Rossana Berardi ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Tumor Angiogenesis ◽  
Targeted Therapies ◽  
Renal Cell ◽  
Mammalian Target Of Rapamycin ◽  
Phosphatidylinositol 3 Kinase ◽  
Von Hippel Lindau ◽  
Angiogenesis Process ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) plays a crucial role in tumor angiogenesis. VEGF expression in metastatic renal cell carcinoma (mRCC) is mostly regulated by hypoxia, predominantly via the hypoxia-induced factor (HIF)/Von Hippel-Lindau (VHL) pathway. Advances in our knowledge of VEGF role in tumor angiogenesis, growth, and progression have permitted development of new approaches for the treatment of mRCC, including several agents targeting VEGF and VEGF receptors: tyrosine kinase pathway, serine/threonine kinases,α5β1-integrin, deacetylase, CD70, mammalian target of rapamycin (mTOR), AKT, and phosphatidylinositol 3′-kinase (PI3K). Starting from sorafenib and sunitinib, several targeted therapies have been approved for mRCC treatment, with a long list of agents in course of evaluation, such as tivozanib, cediranib, and VEGF-Trap. Here we illustrate the main steps of tumor angiogenesis process, defining the pertinent therapeutic targets and the efficacy and toxicity profiles of these new promising agents.

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