scholarly journals Calcitriol inhibits migration and invasion of renal cell carcinoma cells by suppressing Smad2/3‐, STAT3‐ and β‐catenin‐mediated epithelial‐mesenchymal transition

2020 ◽  
Vol 111 (1) ◽  
pp. 59-71 ◽  
Author(s):  
Shen Xu ◽  
Zhi‐Hui Zhang ◽  
Lin Fu ◽  
Jin Song ◽  
Dong‐Dong Xie ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Mesenchymal Transition

scholarly journals TNF-α Induces Epithelial–Mesenchymal Transition of Renal Cell Carcinoma Cells via a GSK3β-Dependent Mechanism

2012 ◽  
Vol 10 (8) ◽  
pp. 1109-1119 ◽  
Author(s):  
Ming-Yi Ho ◽  
Shye-Jye Tang ◽  
Mei-Jen Chuang ◽  
Tai-Lung Cha ◽  
Jing-Yao Li ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Tnf Α ◽  
Dependent Mechanism

scholarly journals Regulation of Oncogenic Targets by the Tumor-Suppressive miR-139 Duplex (miR-139-5p and miR-139-3p) in Renal Cell Carcinoma

Biomedicines ◽  
2020 ◽  
Vol 8 (12) ◽  
pp. 599
Author(s):  
Reona Okada ◽  
Yusuke Goto ◽  
Yasutaka Yamada ◽  
Mayuko Kato ◽  
Shunichi Asai ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Epithelial Mesenchymal Transition ◽  
Ectopic Expression ◽  
Molecular Pathogenesis ◽  
Molecular Networks ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Passenger Strand

We previously found that both the guide and passenger strands of the miR-139 duplex (miR-139-5p and miR-139-3p, respectively) were downregulated in cancer tissues. Analysis of TCGA datasets revealed that low expression of miR-139-5p (p < 0.0001) and miR-139-3p (p < 0.0001) was closely associated with 5-year survival rates of patients with renal cell carcinoma (RCC). Ectopic expression assays showed that miR-139-5p and miR-139-3p acted as tumor-suppressive miRNAs in RCC cells. Here, 19 and 22 genes were identified as putative targets of miR-139-5p and miR-139-3p in RCC cells, respectively. Among these genes, high expression of PLXDC1, TET3, PXN, ARHGEF19, ELK1, DCBLD1, IKBKB, and CSF1 significantly predicted shorter survival in RCC patients according to TCGA analyses (p < 0.05). Importantly, the expression levels of four of these genes, PXN, ARHGEF19, ELK1, and IKBKB, were independent prognostic factors for patient survival (p < 0.05). We focused on PXN (paxillin) and investigated its potential oncogenic role in RCC cells. PXN knockdown significantly inhibited cancer cell migration and invasion, possibly by regulating epithelial–mesenchymal transition. Involvement of the miR-139-3p passenger strand in RCC molecular pathogenesis is a new concept. Analyses of tumor-suppressive-miRNA-mediated molecular networks provide important insights into the molecular pathogenesis of RCC.

scholarly journals Expression of lactate dehydrogenase C correlates with poor prognosis in renal cell carcinoma

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769596 ◽  
Author(s):  
Yibo Hua ◽  
Chao Liang ◽  
Jundong Zhu ◽  
Chenkui Miao ◽  
Yajie Yu ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Lactate Dehydrogenase ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Poor Prognosis ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Lactate Dehydrogenase C

Lactate dehydrogenase C is an isoenzyme of lactate dehydrogenase and a member of the cancer–testis antigens family. In this study, we aimed to investigate the expression and functional role of lactate dehydrogenase C and its basic mechanisms in renal cell carcinoma. First, a total of 133 cases of renal cell carcinoma samples were analysed in a tissue microarray, and Kaplan–Meier survival curve analyses were performed to investigate the correlation between lactate dehydrogenase C expression and renal cell carcinoma progression. Lactate dehydrogenase C protein levels and messenger RNA levels were significantly upregulated in renal cell carcinoma tissues, and the patients with positive lactate dehydrogenase C expression had a shorter progression-free survival, indicating the oncogenic role of lactate dehydrogenase C in renal cell carcinoma. In addition, further cytological experiments demonstrated that lactate dehydrogenase C could prompt renal cell carcinoma cells to produce lactate, and increase metastatic and invasive potential of renal cell carcinoma cells. Furthermore, lactate dehydrogenase C could induce the epithelial–mesenchymal transition process and matrix metalloproteinase-9 expression. In summary, these findings showed lactate dehydrogenase C was associated with poor prognosis in renal cell carcinoma and played a pivotal role in the migration and invasion of renal cell carcinoma cells. Lactate dehydrogenase C may act as a novel biomarker for renal cell carcinoma progression and a potential therapeutic target for the treatment of renal cell carcinoma.

Nobiletin inhibits hypoxia‐induced epithelial‐mesenchymal transition in renal cell carcinoma cells

2018 ◽  
Vol 120 (2) ◽  
pp. 2039-2046 ◽  
Author(s):  
Feng Liu ◽  
Siqi Zhang ◽  
Min Yin ◽  
Lihua Guo ◽  
Mingzhu Xu ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Mesenchymal Transition

scholarly journals Knockdown of Collagen Triple Helix Repeat Containing-1 Inhibits the Proliferation and Epithelial-to-Mesenchymal Transition in Renal Cell Carcinoma Cells

2016 ◽  
Vol 24 (6) ◽  
pp. 477-485 ◽  
Author(s):  
Xue-fei Jin ◽  
Hai Li ◽  
Shi Zong ◽  
Hong-yan Li
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Triple Helix ◽  
Epithelial To Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Collagen Triple Helix

Collagen triple helix repeat containing-1 (CTHRC1), a secreted glycoprotein, is frequently upregulated in human cancers. However, the functional role of CTHRC1 in renal cell carcinoma (RCC) remains unclear. Thus, the aim of this study was to explore the role of CTHRC1 in RCC. Our results demonstrated that CTHRC1 was upregulated in RCC tissues and cell lines. Knockdown of CTHRC1 significantly inhibits the proliferation in RCCs. Furthermore, knockdown of CTHRC1 significantly inhibited the epithelial-to-mesenchymal transition (EMT) process in RCCs, as well as suppressed RCC cell migration and invasion. Mechanistically, knockdown of CTHRC1 inhibited the expression of β-catenin, c-Myc, and cyclin D1 in RCC cells. In conclusion, the results of the present study indicated that CTHRC1 downregulation inhibited proliferation, migration, EMT, and β-catenin expression in RCC cells. Therefore, CTHRC1 may be a potential therapeutic target for the treatment of RCC.

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