scholarly journals Dual Strands of Pre-miR-149 Inhibit Cancer Cell Migration and Invasion through Targeting FOXM1 in Renal Cell Carcinoma

2017 ◽  
Vol 18 (9) ◽  
pp. 1969 ◽  
Author(s):  
Atsushi Okato ◽  
Takayuki Arai ◽  
Yasutaka Yamada ◽  
Sho Sugawara ◽  
Keiichi Koshizuka ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Migration ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Renal Cell ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Cell Migration And Invasion

scholarly journals Tumour-suppressivemicroRNA-29sdirectly regulateLOXL2expression and inhibit cancer cell migration and invasion in renal cell carcinoma

FEBS Letters ◽  
2015 ◽  
Vol 589 (16) ◽  
pp. 2136-2145 ◽  
Author(s):  
Rika Nishikawa ◽  
Takeshi Chiyomaru ◽  
Hideki Enokida ◽  
Satoru Inoguchi ◽  
Tomoaki Ishihara ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Migration ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Renal Cell ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Cell Migration And Invasion

MP23-08 MICRORNA-29S INHIBITS CANCER CELL MIGRATION AND INVASION VIA TARGETING FOCAL ADHESION PATHWAYS IN RENAL CELL CARCINOMA

2014 ◽  
Vol 191 (4S) ◽  
Author(s):  
Hideki Enokida ◽  
Tomokazu Yonezawa ◽  
Takeshi Chiyomaru ◽  
Hirofumi Yoshino ◽  
Toshihiko Itesako ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Migration ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Focal Adhesion ◽  
Renal Cell ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Cell Migration And Invasion

scholarly journals Elevated MTA1 induced the migration and invasion of renal cell carcinoma through the NF-κB pathway

BMC Urology ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Cai Lv ◽  
Yuan Huang ◽  
Qingqing Lei ◽  
Zhenxiang Liu ◽  
Shixing Shen ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Migration ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Normal Tissue ◽  
Negative Control ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Interfering Rna ◽  
E Cadherin

Abstract Background The metastasis-associated gene 1 (MTA1) has been extensively reported as a crucial oncogene, and its abnormal expression has been associated with the progression of numerous cancers. However, the role of MTA1 in renal cell carcinoma (RCC) progression and metastasis remains unclear. Herein, we investigated the expression of MTA1 and its role in RCC. Methods 109 matched clear cell RCCs (ccRCCs) and corresponding normal tissue samples were analyzed via immunohistochemistry to test the expression of MTA1. Human A498 cell lines were transfected with pcDNA3.1-Flag (control) or Flag-MTA1 to overexpress MTA1 or with specific interfering RNA (si-MTA1) or specific interfering negative control to knockdown MTA1 expression. Transfected cells were used in wound healing and transwell invasion assay. Quantitative real time polymerase chain reaction was used to assess the effect of MTA1 on MMP2/MMP9 and E-cadherin gene expression. Western blot was used to qualify the phosphorylation of p65. Results Herein, we found a significantly increased expression of MTA1 in 109 ccRCCs, compared to the corresponding normal tissue. In addition, the overexpression of MTA1 in A498 cells facilitated cell migration and invasion, while the down-regulation of MTA1 expression using specific interfering RNA sequences could decrease cell migration and invasion. Furthermore, we showed that MTA1 is up-regulated in ccRCCs, which contributes to the migration and invasion of human kidney cancer cells by mediating the expression of MMP2 and MMP9 through the NF-κB signaling pathway. Similarly, we found that MTA1 could regulate E-cadherin expression in RCCs. Conclusions MTA1 is overexpressed in RCC and is involved in the progression of RCC through NF-κB.

scholarly journals Upregulated circPDK1 Promotes RCC Cell Migration and Invasion by Regulating the miR-377-3P-NOTCH1 Axis in Renal Cell Carcinoma

2020 ◽  
Vol Volume 13 ◽  
pp. 11237-11252
Author(s):  
Zhenlin Huang ◽  
Yinghui Ding ◽  
Lu Zhang ◽  
Siyuan He ◽  
Zhankui Jia ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Migration ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Migration And Invasion ◽  
Cell Migration And Invasion

scholarly journals The RabGEF ALS2 is a hypoxia inducible target associated with the acquisition of aggressive traits in tumor cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Solange Rivas ◽  
Patricio Silva ◽  
Montserrat Reyes ◽  
Hugo Sepúlveda ◽  
Luis Solano ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Migration ◽  
Tumor Cell ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Proximal Promoter ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Tumor Cell Migration ◽  
Rab Protein

AbstractTumor hypoxia and the hypoxia inducible factor-1, HIF-1, play critical roles in cancer progression and metastasis. We previously showed that hypoxia activates the endosomal GTPase Rab5, leading to tumor cell migration and invasion, and that these events do not involve changes in Rab protein expression, suggesting the participation of intermediate activators. Here, we identified ALS2, a guanine nucleotide exchange factor that is upregulated in cancer, as responsible for increased Rab5-GTP loading, cell migration and metastasis in hypoxia. Specifically, hypoxia augmented ALS2 mRNA and protein levels, and these events involved HIF-1α-dependent transcription, as shown by RNAi, pharmacological inhibition, chromatin immunoprecipitation and bioinformatics analyses, which identified a functional HIF-1α-binding site in the proximal promoter region of ALS2. Moreover, ALS2 and Rab5 activity were elevated both in a model of endogenous HIF-1α stabilization (renal cell carcinoma) and by following expression of stable non-hydroxylatable HIF-1α. Strikingly, ALS2 upregulation in hypoxia was required for Rab5 activation, tumor cell migration and invasion, as well as experimental metastasis in C57BL/6 mice. Finally, immunohistochemical analyses in patient biopsies with renal cell carcinoma showed that elevated HIF-1α correlates with increased ALS2 expression. Hence, this study identifies ALS2 as a novel hypoxia-inducible gene associated with tumor progression and metastasis.

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