MicroRNA-92a promotes cell viability and invasion in cervical cancer via directly targeting Dickkopf-related protein 3
Authors: Chunying Liu
Jiawei Rong
Na Li
Shaohua Yu
Lichun Chen
Shengtian Luo
Journal: Experimental and therapeutic medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: Dickkopf-related protein 3; cervical cancer; invasion; microRNA; viability.
Affiliations: Department of Obstetrics and Gynecology, General Hospital of Daqing Oil Field, Daqing, Heilongjiang 163001, P.R. China.

Abstract:  MicroRNA-92a (miR-92a) was recently reported to have an oncogenic role in cervical cancer; however, the underlying mechanism remains largely unclear. The present study aimed to investigate the expression, clinical significance and regulatory mechanism of miR-92a in cervical cancer. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) data indicated that miR-92a was significantly upregulated in cervical cancer tissues compared with matched adjacent non-tumor tissues (P&lt;0.01). High expression of miR-92a was significantly associated with poor differentiation (P=0.031), advanced clinical stage (P=0.011) and lymph node metastasis (P=0.014), but not associated with age, tumor size and distant metastasis. Knockdown of miR-92a significantly inhibited the viability and invasion of cervical cancer HeLa cells, while overexpression of miR-92a significantly enhanced HeLa cell viability and invasion (P&lt;0.01). Luciferase reporter assay identified Dickkopf-related protein 3 (DKK3) as a target gene of miR-92a, and the protein expression of DKK3 was negatively regulated by miR-92a in HeLa cells. Furthermore, overexpression of DKK3 significantly eliminated the stimulative effects of miR-92a on HeLa cell viability and invasion (P&lt;0.01). Additionally, DKK3 was significantly downregulated in cervical cancer tissues compared with adjacent non-tumor tissues (P&lt;0.01), inversely correlated to the miR-92a levels in cervical cancer tissues (P&lt;0.01). In summary, the present study indicated that miR-92a promotes cell viability and invasion in cervical cancer, partly at least, via inhibiting the protein expression of DKK3. Therefore, the present study highlights the clinical significance of the miR-92a/DKK3 axis in cervical cancer. 

Retracted: No

PubPeer comments:
null, 
 Good afternoon, This is Lluis Fajas, the first author of this paper. First of all, I am sorry for the delayed reply. Second, I feel very uncomfortable not knowing with whom I am discussing. And third, I want to address the subject that has been raised, regarding the PPARg western blot that is shared with other papers. This blot is coming from a unique and very clean experiment of preadipocyte differentiation. In this experiment the samples were collected and blotted against several proteins involved in cell cycle, including cyclin D3, cyclin A, cyclin E, E2F1, E2F4. The aim was to analyze the participation of these proteins in the differentiation process. The expression of PPARg was only used as a control of differentiation. In each individual paper, the expression of the concerned protein is shown, together with the control (PPARg). Please let me insist, all the blots shown in the different papers are the same experiment. This is the reason why the PPARg blot (common to all) is shown several times. Have a nice day , 
 If this is the same control experiment (according to Dr. Fajas own words), why are the days of differentiation different in each paper? , 
 This is a mistake. ,