MicroRNA-138 inhibits proliferation, migration and invasion through targeting hTERT in cervical cancer
Authors: Dan Fei
Mingyue Zhang
Na Zhou
Shan Zong
Ying Yue
Journal: Oncology Letters (2016)
Discipline: CLINICAL MEDICINE
Keywords: cervical cancer; human telomerase reverse transcriptase; microRNA-138; microRNAs.
Affiliations: Department of Obstetrics and Gynecology, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China., Department of Ultrasonography, China-Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China.

Abstract:  A growing body of evidence suggests that microRNA-138 (miR-138) functions as a tumor suppressor, and is involved in tumor initiation, development and metastasis in certain types of human cancers. However, the function and underlying molecular mechanism of miR-138 in cervical cancer remains unclear. Therefore, the purpose of the present study was to investigate the clinical significance of miR-138 expression in cervical cancer, and to evaluate its role and underlying mechanisms in cervical cancer. The present study indicated that miR-138 expression was significantly downregulated in cervical cancer tissues and cell lines, and that the low miR-138 expression was negatively associated with advanced FIGO stage and lymph node metastasis (P&lt;0.01). Functional analyses indicated that the overexpression of miR-138 in cervical cancer cells inhibited cell proliferation, migration and invasion, induced cell apoptosis in vitro, and suppressed tumor growth in a nude mice model. Luciferase reporter assays confirmed that human telomerase reverse transcriptase was a novel target gene of miR-138. The findings of the present study suggested that miR-138 could be a potential candidate for cervical cancer therapeutics. 

Retracted: No

PubPeer comments:
 Fig 3.  (A) A cell **migration** assay was performed in MCF-7 cells transfected with miR-29a mimics or Robo1-specific siRNA, or cotransfected with miR-29a mimics and Robo1 plasmid. The control comprised MCF-7 cells without any transfection. (B) A cell** invasion** assay was performed in MCF-7 cells transfected with miR-29a mimics or Robo1-specific siRNA, or cotransfected with miR-29a mimics and Robo1 plasmid. ![file] I set up a spreadsheet to include the various papers using this versatile suite of Transwell images to represent all possible combinations of cell-lines and treatments. This is the 46th manifestation. For comparison: Fig 3 C D from [Zhang et al (2016)] .  Transwell assay were performed to examine the migratory and invasive capacities of Saos-2 and U2OS cells transfected with miR-205 mimic or miR-negative control (NC) mimic , and Fig 7C D,  Transwell assay were performed to examine cell migration and invasion of MG63 or U2OS cells transfected with miR-205 mimic, or co-transfected with miR-205 mimic and RUNX2 plasmid . ![] Figs 4D, 6D from [Xia et al (2016)] . ![] Also *[above]* Fig 4C from [Lai, Chen Li (2015)] .  a Transwell assay were performed to examine the cell proliferation of AGS cells transfected with miR-133a mimics, miR-133a inhibitor, or co-transfected with miR-133a mimics and FSCN1 plasmid. Control: AGS cells without any transfection. *[below]* Figs 3(B), 6(B) from [Shi et al (2015)] .  Transwell assay was performed to determine the invasive capacity of the Saos-2 and U-2 OS cells transfected with NC scramble miRNA or miR-204 mimics, respectively. Control, Saos-2 and U-2 OS cells without any transfection ...  Transwell assay was performed to determine the invasive capacity of the Saos-2 and U-2 OS cells transfected with Sirt1 siRNA or co-transfected with miR-204 mimics and the Sirt1 plasmid, respectively. Control, Saos-2 and U-2 OS cells without any transfection . ![file] ,