scholarly journals microRNA-145 inhibits cell proliferation, migration and invasion by targeting matrix metallopeptidase-11 in renal cell carcinoma

2014 ◽  
Vol 10 (1) ◽  
pp. 393-398 ◽  
Author(s):  
DEYAO WU ◽  
MIN LI ◽  
LINMAO WANG ◽  
YUNFENG ZHOU ◽  
JIAN ZHOU ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Migration And Invasion ◽  
Matrix Metallopeptidase

The expression of Cullin1 is increased in renal cell carcinoma and promotes cancer cell proliferation, migration, and invasion

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 ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Renal Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation

scholarly journals LncRNA POU3F3 Promotes Cancer Cell Proliferation, Migration, and Invasion in Renal Cell Carcinoma by Downregulating LncRNA GAS5

2021 ◽  
pp. 1-7
Author(s):  
Lei Zhang ◽  
Cezheng Wang ◽  
Min Ma
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
In Situ Hybridization ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Tumor Tissues ◽  
Lncrna Gas5

<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.

scholarly journals miR-129-5p inhibits clear cell renal cell carcinoma cell proliferation, migration and invasion by targeting SPN

2020 ◽  
Author(s):  
Bin Gao ◽  
Lijuan Wang ◽  
Yubo Zhang ◽  
Na Zhang ◽  
Miaomiao Han ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Clear Cell ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Cell Renal Cell Carcinoma ◽  
Regulated Expression ◽  
Ccrcc Cell

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.

scholarly journals Ubenimex inhibits cell proliferation, migration and invasion in renal cell carcinoma: The effect is autophagy-associated

2014 ◽  
Vol 33 (3) ◽  
pp. 1372-1380 ◽  
Author(s):  
SHUAI LIU ◽  
FANG XIE ◽  
HAFENG WANG ◽  
ZHENG LIU ◽  
XIAOWEN LIU ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Migration And Invasion

scholarly journals SNHG12 Regulated by KMT2B Participates in the Pathogenesis of Renal Cell Carcinoma via E2F1/CEP55

2022 ◽  
Author(s):  
Jia-fu Feng ◽  
Jun Wang ◽  
Gang Xie ◽  
Yao-dong Wang ◽  
Xiao-han Li ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Promoter Region ◽  
Xenograft Model ◽  
Tumor Formation ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mouse Xenograft Model

Abstract Objective: This study is to investigate the regulation of long non-coding RNA (lncRNA) SNHG12 promoter methylation modification by KMT2B and the mechanism of SNHG12 in the development of renal cell carcinoma (RCC) involving E2F1/CEP55 axis.Methods: TCGA and GEO databases were used to predict the involvement of SNHG12 in RCC. Knockdown of SNHG12/E2F1/CEP55 was performed. Next, SNHG12 expression and other mRNAs were analyzed by RT-qPCR. Subsequently, CCK-8 was used to detect cell proliferation. Wound healing test and Transwell assay was used to detect cell migration and invasion, respectively. The vascularization of HUVEC was explored by in vitro pseudotubule formation. CHIP was used to detect H3K4me3 in SNHG12 promoter region. The binding of E2F1 and CEP55 promoter region was analyzed with CHIP and dual luciferase reporter assay. RIP was used to detect the binding of SNHG12 and E2F1. Finally, the effect of SNHG12 on the tumor formation and angiogenesis of RCC was assessed in nude mouse xenograft model.Results: Bioinformatics analysis showed that SNHG12 was highly expressed in RCC tissues and cells, and it was related to the poor prognosis of RCC patients. SNHG12 knockdown significantly inhibited RCC cell proliferation, migration, and invasion and HUVEC angiogenesis. KMT2B up-regulated SNHG12 through modifying H3K4me3 in its promoter region. In addition, SNHG12 promoted CEP55 expression by recruiting the transcription factor E2F1. Knockdown of SNHG12 blocked E2F1 recruitment, thereby down-regulating the expression of CEP55, and inhibited tumor formation and angiogenesis of RCC cells in nude mice.Conclusion: KMT2B up-regulates SNHG12 via the modification of H3K4me3 in its promoter region. SNHG12 recruits E2F1 to promote the expression of CEP55, and ultimately promotes RCC cell proliferation, migration, and invasion and HUVEC angiogenesis.

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