scholarly journals MicroRNA-384 Inhibits the Growth and Invasion of Renal Cell Carcinoma Cells by Targeting Astrocyte Elevated Gene 1

2018 ◽  
Vol 26 (3) ◽  
pp. 457-466 ◽  
Author(s):  
Haitao Song ◽  
Yanwei Rao ◽  
Gang Zhang ◽  
Xiangbo Kong
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Bioinformatic Analysis ◽  
Carcinoma Cells ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Antitumor Effects ◽  
Potential Therapeutic Target

MicroRNAs (miRNAs) are emerging as pivotal regulators in the development and progression of various cancers, including renal cell carcinoma (RCC). MicroRNA-384 (miR-384) has been found to be an important cancer-related miRNA in several types of cancers. However, the role of miR-384 in RCC remains unclear. In this study, we aimed to investigate the potential function of miR-384 in regulating tumorigenesis in RCC. Here we found that miR-384 was significantly downregulated in RCC tissues and cell lines. Overexpression of miR-384 significantly inhibited the growth and invasion of RCC cells, whereas inhibition of miR-384 had the opposite effects. Bioinformatic analysis and luciferase reporter assay showed that miR-384 directly targeted the 3′-untranslated region of astrocyte elevated gene 1 (AEG-1). Further data showed that miR-384 could negatively regulate the expression of AEG-1 in RCC cells. Importantly, miR-384 expression was inversely correlated with AEG-1 expression in clinical RCC specimens. Moreover, miR-384 regulates the activation of Wnt signaling. Overexpression of AEG-1 significantly reversed the antitumor effects of miR-384. Overall, these findings suggest that miR-384 suppresses the growth and invasion of RCC cells via downregulation of AEG-1, providing a potential therapeutic target for the treatment of RCC.

scholarly journals Role of SIRT1/AMPK signaling in the proliferation, migration and invasion of renal cell carcinoma cells

2021 ◽  
Vol 45 (6) ◽  
Author(s):  
Xin Wang ◽  
Youlu Lu ◽  
Zhouting Tuo ◽  
Huan Zhou ◽  
Ying Zhang ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Ampk Signaling

scholarly journals Reply to Comment on “Kadomoto, S. et al. Tumor-Associated Macrophages Induce Migration of Renal Cell Carcinoma Cells via Activation of the CCL20-CCR6 Axis” Cancers 2020 12, 89

Cancers ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 354
Author(s):  
Kadomoto ◽  
Izumi ◽  
Hiratsuka ◽  
Nakano ◽  
Naito ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Tumor Microenvironment ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Culture System ◽  
Staining Intensity ◽  
Carcinoma Cells ◽  
Definite Difference ◽  
M1 And M2 Macrophages

We appreciate Zins and Abraham [1] commenting on our paper studying the role of the CCL20-CCR6 axis on renal cell carcinoma (RCC) cells [2]. As they pointed out, our study has certain limitations. Although M1- and M2-types cannot be separated clearly and a consecutive change of character might exist between them, it has been reported that plural specific markers express on M1- and M2-types. Unfortunately, a definite difference between M1 and M2 macrophages was not confirmed in our study. For more differentiation, multiple stimulations, such as suggested in the comments of Zins and Abraham, might be needed. Hence, we needed to expediently use “M1-like” and “M2-like” to mention specific status of these macrophage-like cells. Meanwhile, CCL20 expression levels of M2-like-THP-1 cells co-cultured with RCC cells were dramatically increased compared with parental THP-1 cells, indicating that certain stimulations within the tumor microenvironment rather than theoretical stimulations make macrophages differentiated; however, further studies are needed to clarify this mechanism using a more appropriate co-culture system mimicking the tumor microenvironment. Immunohistochemistry of CCL20 and M2 markers will help to better understand the role of tissue infiltrating macrophages, even tissue CD68 staining intensity itself was reported to correlate with prognosis of RCC patients [3]. [...]

scholarly journals Effect of perineoplasm perinephric adipose tissues on migration of clear cell renal cell carcinoma cells: a potential role of WNT signaling

Oncotarget ◽  
2016 ◽  
Vol 7 (33) ◽  
pp. 53277-53288 ◽  
Author(s):  
Xiaolin Zi ◽  
Achim Lusch ◽  
Christopher A. Blair ◽  
Zhamshid Okhunov ◽  
Noriko N. Yokoyama ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Wnt Signaling ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Potential Role ◽  
Clear Cell ◽  
Carcinoma Cells ◽  
Cell Renal Cell Carcinoma ◽  
Adipose Tissues

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.

scholarly journals The natural extract degalactotigonin exerts antitumor effects on renal cell carcinoma cells through repressing YAP

2020 ◽  
Vol 9 (12) ◽  
pp. 7550-7561
Author(s):  
Yuning Wang ◽  
Tianyu Hong ◽  
Linbao Chen ◽  
Chuanmin Chu ◽  
Jiangbo Zhu ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Carcinoma Cells ◽  
Antitumor Effects ◽  
Natural Extract

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.

306 ROLE OF EPHA2 IN MALIGNANT CELLULAR BEHAVIOR IN RENAL CELL CARCINOMA CELLS

2013 ◽  
Vol 189 (4S) ◽  
Author(s):  
Min Chul Cho ◽  
Sung Yong Cho ◽  
Seung Bae Lee ◽  
Cheol Kwak ◽  
Hae Won Lee ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Carcinoma Cells ◽  
Cellular Behavior
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