scholarly journals Hypoxia-Induced Placenta-Specific microRNA (miR-512-3p) Promotes Hepatocellular Carcinoma Progression by Targeting Large Tumor Suppressor Kinase 2

2020 ◽  
Vol Volume 13 ◽  
pp. 6073-6083
Author(s):  
Bohan Zhang ◽  
Liang Huang ◽  
Jiangbo Tu ◽  
Tianming Wu
2018 ◽  
Vol 51 (3) ◽  
pp. 1179-1192 ◽  
Author(s):  
Li Li Han ◽  
Xiao Ran Yin ◽  
Shu Qun Zhang

Background/Aims: Previous studies have confirmed that microRNAs are involved in the metastasis and epithelial–mesenchymal transition (EMT) of malignancies. In this study, we examined whether miR-650 promotes the migration, invasion, and EMT of hepatocellular carcinoma (HCC) cells by targeting the large tumor suppressor kinase 2 gene (LATS2). Methods: qRT-PCR was used to detect expression of miR-650 in HCC tissues and paired normal tissues. MTT and Transwell assay were used to observe the effect of miR-650 on proliferation, migration and invasion of HCC cells. Western blot assay and Immunohistochemistry were performed to demonstrate association between miR-650 expression level and epithelial-mesenchymal transition (EMT) related protein. Mechanistically, Reporter luciferase assay was performed to reveal whether large tumor suppressor kinase 2 (LATS2) was a direct target of miR-650 in HCC cells. Results: We observed that miR-650 levels were largely up-regulated in HCC tissues, and that the increased expression was closely associated with the adverse clinical features of HCC patients. Additionally, the expression of LATS2, which was identified as a direct target of miR-650, can counteract the effects of miR-650 in HCC. Furthermore, we demonstrated that high miR-650 expression levels and low LATS2 expression levels in tumors may indicate a poor prognosis for HCC patients. Conclusion: In conclusion, the miR-650/LATS2 pathway may serve as a novel prognostic biomarker and an attractive therapeutic target for HCC patients.


Bioengineered ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 12357-12371
Author(s):  
Zexiang Jiang ◽  
Weiping Xia ◽  
Guoyu Dai ◽  
Bo Zhang ◽  
Yang Li ◽  
...  

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