scholarly journals Erratum of the article: MTHFD2 Overexpression Predicts Poor Prognosis in Renal Cell Carcinoma and is Associated with Cell Proliferation and Vimentin-Modulated Migration and Invasion

2019 ◽  
Vol 52 (6) ◽  
pp. 1589-1589
Tumor Biology ◽  
2016 ◽  
Vol 37 (9) ◽  
pp. 12823-12831 ◽  
Author(s):  
Ji-Gen Ping ◽  
Fei Wang ◽  
Jin-Xian Pu ◽  
Ping-Fu Hou ◽  
Yan-Su Chen ◽  
...  

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769596 ◽  
Author(s):  
Yibo Hua ◽  
Chao Liang ◽  
Jundong Zhu ◽  
Chenkui Miao ◽  
Yajie Yu ◽  
...  

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.


2021 ◽  
pp. 1-7
Author(s):  
Lei Zhang ◽  
Cezheng Wang ◽  
Min Ma

<b><i>Background:</i></b> LncRNAs play regulatory roles in diverse nephrological disorders, including renal cancer. Overexpression of lncRNA POU3F3 (POU3F3) has only been reported in esophageal squamous-cell carcinomas, indicating POU3F3 may be an oncogene in this disease. LncRNA GAS5 (GAS5) was reported to be a suppressor in various tumors. However, the roles and underlying mechanism of POU3F3 and GAS5 involved in renal cell carcinoma (RCC) remain unknown. <b><i>Methods:</i></b> Real-time quantitative PCR and in situ hybridization were performed to determine the expression of POU3F3 and GAS5 in paired tumor and adjacent healthy tissues donated by 68 RCC patients. The prognostic values of POU3F3 and GAS5 for RCC were analyzed by performing a 5-year follow-up study. Overexpression of POU3F3 and GAS5 was achieved in RCC cells to explore the interactions between them. Transwell assay and cell proliferation assay were performed to evaluate the role of POU3F3 and GAS5 in regulating RCC cell proliferation, migration, and invasion. <b><i>Results:</i></b> In the present study, we found that POU3F3 was upregulated while GAS5 was downregulated in tumor tissues than that in adjacent healthy tissues of patients with RCC. In situ hybridization analysis showed that POU3F3 was mostly expressed in tumor tissues, while GAS5 was mostly expressed in adjacent healthy tissues. High level of POU3F3 and low level of GAS5 were closely correlated with poor prognosis of RCC patients. Expression levels of POU3F3 and GAS5 were significantly and inversely correlated in tumor tissues but not in adjacent healthy tissues of RCC patients. Overexpression of POU3F3 mediated the downregulation of GAS5 in RCC cells, while GAS5 overexpression failed to significantly affect POU3F3 expression. Overexpression of POU3F3 led to promoted, while GAS5 overexpression led to inhibited proliferation, migration, and invasion of RCC cells. In addition, GAS5 overexpression attenuated the enhancing effects of POU3F3 overexpression on cancer cell proliferation, migration, and invasion. <b><i>Conclusion:</i></b> POU3F3 promoted cell proliferation, migration, and invasion in RCC possibly by downregulating GAS5.


2020 ◽  
Author(s):  
Bin Gao ◽  
Lijuan Wang ◽  
Yubo Zhang ◽  
Na Zhang ◽  
Miaomiao Han ◽  
...  

Abstract Objective: Our study aims to investigate the mechanism of the miR-129-5p/SPN axis in clear cell renal cell carcinoma (ccRCC), providing a novel direction for the targeted therapy of ccRCC. Methods: Bioinformatics methods were implemented to find the differentially expressed genes (DEGs) associated with ccRCC from TCGA database. qRT-PCR was performed to detect miR-129-5p and SPN mRNA expression, while western bot was carried out for the detection of protein expression of SPN. Bioinformatics analysis was used to predict the binding sites of miR-129-5p on SPN 3’UTR, while dual-luciferase assay was conducted to verify their binding relationship. CCK-8 assay, colony formation assay, wound healing assay and Transwell assay were employed to measure ccRCC cell proliferative ability, cell formation ability, cell migratory and invasive abilities. Results: miR-129-5p exhibited a significantly down-regulated expression level in ccRCC, while SPN showed a remarkably up-regulated expression level. Overexpressed miR-129-5p inhibited ccRCC cell proliferative, invasive and migratory capacities. Dual-luciferase assay confirmed that there was a binding relationship between miR-129-5p and SPN. Additionally, overexpressing miR-129-5p markedly reduced SPN expression in tumor cells, and attenuated the promoting effect of SPN on cell proliferation, migration and invasion. Conclusion: Our study proves the regulatory effect of the miR-129-5p/SPN axis in ccRCC, and provides a novel potential target for precise treatment of patients with ccRCC.


2014 ◽  
Vol 33 (3) ◽  
pp. 1372-1380 ◽  
Author(s):  
SHUAI LIU ◽  
FANG XIE ◽  
HAFENG WANG ◽  
ZHENG LIU ◽  
XIAOWEN LIU ◽  
...  

2021 ◽  
pp. 1-8
Author(s):  
Qianfeng Zhuang ◽  
Min Fan ◽  
Jie Shen ◽  
Zhen Chen ◽  
Dong Xue ◽  
...  

<b><i>Introduction:</i></b> Calpain small subunit 1 (Capns1) has shown its correlation with the metastasis and invasion of hepatocellular carcinoma and intrahepatic cholangiocarcinoma. However, the expression and function of Capns1 in human renal cell carcinoma (RCC) have not been clarified. This study aimed to examine the expression of Capns1 in RCC tissues and cell lines and to assess its role performed in RCC. <b><i>Methods:</i></b> Capns1 expression was evaluated in 75 pairs of RCC and matched adjacent non-tumor tissues by immunohistochemistry. The prognostic value of Capns1 in RCC was assessed by Kaplan-Meier and Cox regression analyses. The action of Capns1 in the proliferation, adhesion, migration, and invasion of RCC cells and the effects on matrix metalloproteinase (MMP) 2 and 9 expression were evaluated after Capns1 silence. <b><i>Results:</i></b> Capns1 expression was significantly higher in RCC tissues compared with the adjacent non-tumor tissues. Multivariate analysis showed that Capns1 overexpression was an independent poor prognostic marker in RCC. The silencing of Capns1 prohibited cell adhesion and impaired the migration and invasion ability of 786-O cells in vitro. Furthermore, Capns1 silence reduced MMP2 and MMP9 expression. <b><i>Conclusion:</i></b> Capns1 overexpression predicts poor prognosis and correlates with tumor progression in RCC. Capns1 expression might serve a prognostic marker and therapeutic target for RCC.


Sign in / Sign up

Export Citation Format

Share Document