miR-196a targets netrin 4 and regulates cell proliferation and migration of cervical cancer cells

2013 ◽  
Vol 440 (4) ◽  
pp. 582-588 ◽  
Author(s):  
Jie Zhang ◽  
Fangxia Zheng ◽  
Gang Yu ◽  
Yanhua Yin ◽  
Qingyang Lu
2016 ◽  
Vol 26 (5) ◽  
pp. 851-858 ◽  
Author(s):  
Xiao Yu ◽  
Weihong Zhao ◽  
Xin Yang ◽  
Zhilian Wang ◽  
Min Hao

ObjectiveThe aim of this study was to examine the relationship between miR-375 expression and the proliferation, apoptosis, and migration of cervical cancer cells. To further explore the potential target gene of miR-375, insulin-like growth factor 1 receptor (IGF-1R) was detected in miR-375 overexpressed and inhibited cervical cancer cells, which clarified the potential mechanism of miR-375 in the growth and development of cervical cancer.MethodsIn a cervical cancer cell line (Caski), miR-375 overexpression and knockdown were achieved by transfection with a synthetic miR-375 mimic or miR-375–targeting inhibitor oligonucleotides, respectively, using siRNA-Mate transfection reagents. Real-time Polymerase Chain Reaction was performed to detect the expression level of miR-375. The functional effects of miR-375 on cell proliferation, migration, and apoptosis were evaluated using a Cell Counting Kit (CCK-8) and through scratch wound tests and apoptosis assays, respectively. Western blotting was performed to detect the expression level of the IGF-1R protein.ResultTransfection with the miR-375 mimic significantly upregulated the expression of miR-375 by approximately 7.76-fold (P< 0.05), reduced cell proliferation and migration (P< 0.05), increased apoptosis (P< 0.05), and decreased the expression of the IGF-1R protein by 24.73% (P< 0.05) compared with the negative control. In contrast, transfection of the miR-375 inhibitor decreased the expression of miR-375 by 14.39% (P< 0.05), significantly increased cell proliferation and migration (P< 0.05), significantly reduced the cell apoptosis (P< 0.05), and upregulated the expression of the IGF-1R protein by 2.29-fold (P< 0.05). The cells transfected with the negative control showed no significant changes compared with the blank control for each parameter (P> 0.05).ConclusionsmiR-375 plays an important role in the tumorigenesis and development of cervical cancer. IGF-1R might represent a target gene of miR-375 in cervical cancer.


RSC Advances ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 5230-5230
Author(s):  
Laura Fisher

Retraction of ‘RNA-sequencing identified miR-3681 as a negative regulator in the proliferation and migration of cervical cancer cells via the posttranscriptional suppression of HGFR’ by Fan Shi et al., RSC Adv., 2019, 9, 22376–22383, DOI: 10.1039/C9RA01785B.


RSC Advances ◽  
2019 ◽  
Vol 9 (39) ◽  
pp. 22376-22383 ◽  
Author(s):  
Fan Shi ◽  
Yingbing Zhang ◽  
Juan Wang ◽  
Jin Su ◽  
Zi Liu ◽  
...  

In this study, RNA-sequencing was used to investigate the differentially expressed miRNAs between cervical cancer tissues and matched adjacent non-tumor tissues.


2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Xin Li ◽  
Li li Liu ◽  
Ju lei Yao ◽  
Kai Wang ◽  
Hao Ai

MicroRNAs (miRNAs) are potential therapeutic targets in endometrial cancer, but the difficulties associated with their delivery to tumor target cells have hampered their applications. Human umbilical cord mesenchymal stem cells (hUCMSCs) have a well-recognized tumor-homing ability, emphasizing the capacity of tumor-targeted delivery of extracellular vesicles. hUCMSCs release extracellular vesicles rich in miRNAs, which play a vital role in intercellular communication. The purpose of this study was to verify a potential tumor suppressor microRNA, miR-302a, and engineered hUCMSC extracellular vesicles enriched with miR-302a for therapy of endometrial cancer. Here, we observed that miR-302a was significantly downregulated in endometrial cancer tissues when compared with adjacent tissues. Overexpression of miR-302a in endometrial cancer cells robustly suppressed cell proliferation and migration. Meanwhile, the proliferation and migration were significantly inhibited in endometrial cancer cells when cultured with miR-302a-loaded extracellular vesicles derived from hUCMSCs. Importantly, our data showed that engineered extracellular vesicles rich in miR-302 significantly inhibited the expression of cyclin D1 and suppressed AKT signaling pathway in endometrial cancer cells. These results suggested that exogenous miR-302a delivered by hUCMSC-derived extracellular vesicles has exciting potential as an effective anticancer therapy.


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