MicroRNA-1292-5p inhibits cell growth, migration and invasion of gastric carcinoma by targeting DEK
Authors: Shuqun Zhang
Lei Dong
Ying Zan
Wentao Hui
Xiaobin Ma
Lingqin Song
Journal: American journal of cancer research (2018)
Discipline: CLINICAL MEDICINE
Keywords: DEK; MicroRNA-1292-5p; gastric carcinoma; migration; proliferation.
Affiliations: Department of Medical Oncology, The Second Affiliated Hospital of Xi'an Jiaotong University Xi'an 710004, Shaanxi, China., Department of Gastroenterology, The Second Affiliated Hospital of Xi'an Jiaotong University Xi'an 710004, Shaanxi, China.

Abstract:  Gastric cancer ranks as the third most lethal cancer worldwide. Although many efforts have been made to identify novel markers for early diagnosis and effective drugs for the treatment of gastric cancer, the outcome is still poor due to delayed diagnosis and lack of therapeutic options. MicroRNAs (miRNAs) play crucial roles during tumorigenesis, and several miRNAs were found to be critical for gastric cancer development, offering promise as therapeutic targets. The results of this study indicate that a novel miRNA, miR-1292-5p, is downregulated both in gastric carcinoma in vivo and in gastric cancer cell lines in vitro. In addition, we showed that attenuation of miR-1292-5p inhibited the growth, migration and invasion of the AGS and SGC-7901 gastric cancer cell lines. Importantly, our results demonstrate that the proto-oncogenic protein DEK is a direct target of miR-1292-5p in gastric carcinoma. Our results therefore demonstrate a tumor suppressor role of miR-1292-5p in gastric carcinoma and hint at the diagnostic and therapeutic potential of the miR-1292-5p/DEK pathway in gastric cancer. 

Retracted: No

PubPeer comments:
 Fig 2  C. Cell migration analysis of normal SGC-7901 AGS cells and SGC-7901 AGS cells overexpressing miR-1292-5p. D. Cell invasion analysis of normal SGC-7901 AGS cells and SGC-7901 AGS cells overexpressing miR-1292-5p. Fig 5  E. Cell migration analysis of normal SGC-7901 AGS cells and SGC-7901 AGS cells transfected with DEK siRNA. F. Cell invasion analysis of normal SGC-7901 AGS cells and SGC-7901 AGS cells transfected with DEK siRNA. Fig 6  D. Cell migration analysis of normal SGC-7901 AGS cells, SGC-7901 AGS cells overexpressing miR-1292-5p, and SGC-7901 AGS cells co-overexpressing miR-1292-5p and DEK. Error bars indicate SD and *indicates P 0.05. E. Cell invasion analysis of normal SGC-7901 AGS cells, SGC-7901 AGS cells overexpressing miR-1292-5p, and SGC-7901 AGS cells co-overexpressing miR-1292-5p and DEK . I have marked some overlaps. ![file] , 
 I have several additional questions about this manuscript.  We used miRNA target prediction software to search for the target genes of miR-1292-5p. TargetScan predicts 2687 transcripts containing one or more target sites for miR-1292-5p. Of course, most of these predictions are false. It would be helpful if the authors could provide more details, such as which prediction software was used, how the results were analyzed, and why the selected target was chosen. miR-1292-5p is not well annotated as a microRNA, and seems to be a very low abundance miRNA. It is not included in the rigorous mirgenedb database. What is the level of this miRNA in the cells? There are several issues with the luciferase reporter assays that at least for me raise the question if these assays were correctly performed or even performed at all. 1) Figure 4B is incorrect (see below). It appears that the miRNA and the putative target have been switched and flipped. Since this figure shows the sequence that was inserted into the dual luciferase reporter, it raises concerns that the wrong sequence may have been used, which would invalidate the results. Could the authors please provide sequencing data for the plasmid, confirming insertion of the correct sequence? 2) The figure legend of Figure 4 states that  Luciferase reporter plasmids were constructed by the insertion of the full-length **NRP1** 3u2019UTR into a region immediately downstream of the luciferase gene. However, NRP1 is a completely different gene from DEK. What was actually inserted into the plasmid, and downstream of which luciferase gene? (There are two.) 3) The details of reporter plasmid construction and use are not mentioned in the methods section. Could the authors please provide detailed methods for these reagents and assays? ![file] Detailed miRNA-specific reverse transcription and quantitative PCR methods are not provided. Could the authors please provide these details including the RT primers and forward and reverse primers for qPCR? ,