MicroRNA-148a inhibits migration and invasion of ovarian cancer cells via targeting sphingosine-1-phosphate receptor 1
Authors: Shanshan Liu
Zhengfang Wen
Shaoru Li
Ying Liu
Shuzhen Zhao
Xiaorui Li
Journal: Molecular Medicine Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNAs; gene silencing; cancer progression; miR-148a; ovarian cancer
Affiliations: Department of Gynecology and Obstetrics, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan 453100, P.R. China., Department of Oncology, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan 453100, P.R. China.

Abstract:  MicroRNAs, a group of small non-coding RNA molecules that are involved in gene silencing, function as fine‚Äëtuning regulators during cancer progression. MicroRNA (miR)-148a has previously been demonstrated to be associated with ovarian cancer. However, whether miR‚Ä?48a influences the migration and invasion of ovarian cancer cells has remained elusive. In the present study, reverse transcription‚Äëquantitative polymerase chain reaction and western blotting were conducted to examine mRNA and protein expression levels, respectively. Luciferase reporter assay was used to determine target relationship, and a Transwell assay was used to study cell migration and invasion. The results of the present study indicated that miR‚Ä?48a expression was markedly downregulated in ovarian cancer tissues compared with that of their matched normal adjacent tissues. In addition, miR‚Ä?48a expression levels were reduced in three ovarian cancer cell lines, SKOV3, OVCAR and A2780, when compared with those of HUM‚ÄëCELL‚Ä?088 normal ovarian epithelial cells. Furthermore, sphingosine‚Ä?‚Äëphosphate receptor 1 (S1PR1), which is upregulated in ovarian cancer tissues and cell lines, was identified as a novel target of miR‚Ä?48a in SKOV3 ovarian cancer cells. The protein expression of S1PR1 was negatively regulated by miR‚Ä?48a in SKOV3 cells. Furthermore, overexpression of miR‚Ä?48a or inhibition of S1PR1 suppressed SKOV3 cell migration and invasion, while restoration of S1PR1 expression reversed the suppressive effect of miR‚Ä?48a upregulation on SKOV3 cell migration and invasion. In conclusion, it was hypothesized that miR‚Ä?48a may potentially be used as a molecular agent for the prevention and treatment of invasion and metastasis in ovarian cancer, while S1PR1 may present a promising target for clinical applications. 

Retracted: Yes

PubPeer comments:
 Fig 4 A,B.  miR-148a inhibits ovarian cancer cell migration and invasion. (A) A cell migration assay was performed to determine the migration capacity of SKOV3 cells transfected with miR-148a mimics, S1PR1 siRNA or co-transfected with miR-148a mimics and S1PR1 plasmid ... (B) A cell invasion assay was performed to determine the cellular invasion capacity of SKOV3 cells transfected with miR-148a mimics, S1PR1 siRNA or co-transfected with miR-148a mimics and S1PR1 plasmid .  For comparison: *[upper]* Figs 4 C D and 5C from [Yang et al (2016)] .  Transwell assays were conducted to examine the cell invasion capacities ofA549 cells transfected with (C) miR-133b mimics and (D) FSCN1 plasmids. Non-transfected A549 cells were used as control ....  Transwell assay were conducted to examine the cell migration and invasion in each group . *[lower]* Fig 5B from [Wang et al (2016)] .  Transwell assay to determine the invasive capacity of U2OS cells transfected with miRu2011101 mimics or cu2011FOS siRNA, or cou2011transfected with miRu2011101 mimics and cu2011FOS plasmid. Magnification, x100. Control: untransfected U2OS cells .  Fig 7 from [Wang et al (2014)] .  Cell invasion assay was performed to determine the effect of miR-195 and CARMA3 on invasion in SW480 and HT29 cells following transfection with an miR-195 mimic or an miR-195 inhibitor, or co-transfected with an miR-195 mimic and CARMA3-pcDNA3.1 .  , 
 Retracted [15 July 2021] . ----------------------------------------- Following the publication of this paper, it was drawn to the Editorsu2019 attention by a concerned reader that certain of the western blotting data shown in Fig. 4A and B were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. ,