scholarly journals miR-133a-3p Functions as a Tumor Suppressor in Colorectal Cancer by Targeting PFKFB3

Author(s):  
Yanjie Zhou ◽  
Lu Jiang ◽  
Yuanjun Cai ◽  
Wendong Tang ◽  
Ke Wang

Abstract Background Recent studies reveal that PFKFB3 plays an important role in tumorigenesis and tumor progression. Our study aims to identify an novel microRNA which can suppress the expression of PFKFB3 and to provide a potential target for tumor therapy. Methods Bioinformatics methods were implemented to explore the expression and clinical significance of PFKFB3 and miR-133a-3p in colorectal cancer (CRC). qRT-PCR was performed to detect PFKFB3, miR-133a-3p, KI67 and MMP9 mRNA expression, while western bot was carried out for the detection of protein expression of PFKFB3, miR-133a-3p, KI67 and MMP9. Bioinformatics analysis was used to predict the binding sites of miR-133a-3p on PFKFB3 3’UTR, while dual-luciferase assay was conducted to validate their binding relationship. CCK-8 assay, KI67 detection, Transwell assay and MMP9 detection were employed to measure CRC cell proliferative and invasive abilities. Results PFKFB3 expression is up-regulated in colorectal cancer, and is significantly associated with poor prognosis. Silencing PFKFB3 could inhibit the proliferation and invasion of colorectal cancer cells. miR-133a-3p is down regulated in colorectal cancer, which has diagnostic value for colorectal cancer. Dual luciferase assay confirmed that PFKFB3 was the direct acting site of miR-133a-3p. Overexpression of miR-133a-3p could significantly reduce the expression of PFKFB3 and inhibit the effect of PFKFB3 on the proliferation and invasion of colorectal cancer cells. Conclusions Our study suggested that miR-133a-3p functions as a novel tumor suppressor in colorectal cancer by targeting PFKFB3.

2021 ◽  
Author(s):  
Yanjie Zhou ◽  
Lu Jiang ◽  
Yuanjun Cai ◽  
Wendong Tang ◽  
Ke Wang

Abstract Background: Recent studies reveal that PFKFB3 plays an important role in tumorigenesis and tumor progression. Our study aims to identify an novel microRNA which can suppress the expression of PFKFB3 and to provide a potential target for tumor therapy.Methods: Bioinformatics methods were implemented to explore the expression and clinical significance of PFKFB3 and miR-133a-3p in colorectal cancer (CRC). qRT-PCR was performed to detect PFKFB3, miR-133a-3p, KI67 and MMP9 mRNA expression, while western bot was carried out for the detection of protein expression of PFKFB3, miR-133a-3p, KI67 and MMP9. Bioinformatics analysis was used to predict the binding sites of miR-133a-3p on PFKFB3 3’UTR, while dual-luciferase assay was conducted to validate their binding relationship. CCK-8 assay, KI67 detection, Transwell assay and MMP9 detection were employed to measure CRC cell proliferative and invasive abilities. Results: PFKFB3 is up-regulated in CRC and significantly associated with poor prognosis. Overexpressed PFKFB3 promotes CRC cell proliferation and invasion. miR-133a-3p is down-regulated and has diagnostic value in CRC. Dual-luciferase assay confirmed that there was a binding relationship between miR-133a-3p and PFKFB3.Overexpressed miR-133a-3p remarkably reduced PFKFB3 expression in CRC cells, weakened the promoting effect of PFKFB3 on cell proliferation and invasion.Conclusions: Our study suggests that miR-133a-3p functions as a novel tumor suppressor in colorectal cancer by targeting PFKFB3.


2015 ◽  
Vol 12 (5) ◽  
pp. 7643-7648 ◽  
Author(s):  
GUANGHUI LIU ◽  
YUANHUA LIU ◽  
ZHEN YANG ◽  
JUNXIA WANG ◽  
DONGYAN LI ◽  
...  

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jing Li ◽  
Rubing Mo ◽  
Linmei Zheng

Abstract Objective Colorectal cancer is one of the most common malignancy in the world. The oncogenesis of colorectal cancer is still not fully elucidated. It was reported that microRNA-490-3p (miR-490-3p) was closely related to the regulation of cancers. However, if miR-490-3p could also affect colorectal cancer and the specific mechanism remains unclear. Methods qRT-PCR was conducted to examine the expression of miR-490-3p. DIANA, miRDB, and TargetScan databases were used to identify target genes. LOVO and SW480 cells were transfected by miR-490-3p mimics and inhibitors. Transwell assay was used to measure cell invasion and migration. Cisplatin and fluorouracil were administered to investigate chemotherapy resistance. Western blot was used to measure TNKS2 protein expression. Binding sites were verified using the double luciferase assay. Results miR-490-3p expression was low in the colorectal cancer cells. The level of miR-490-3p was negatively correlated with cell migration and invasion of cancer cells. miR-490-3p could bind to TNKS2 mRNA 3′UTR directly. miR-490-3p can suppress cell viability and resistance to chemotherapy in colorectal cancer cells through targeting TNKS2. Conclusions miR-490-3p could affect colorectal cancer by targeting TNKS2. This study may provide a potential therapeutic target for colorectal cancer.


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