MicroRNA-133a inhibits proliferation and invasion, and induces apoptosis in gastric carcinoma cells via targeting fascin actin-bundling protein 1
Authors: Ruixin Li
Chen Lai
Zihua Chen
Journal: Molecular Medicine Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: Fascin actin-bundling protein 1 (FSCN1); tumor progression; microRNA (miR)-133a; gastric cancer; proliferation
Affiliations: Department of General Surgery, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.

Abstract:  Fascin actin-bundling protein 1 (FSCN1) is associated with tumor progression. In addition, deregulation of the expression of FSCN1 has been observed in certain types of cancer. However, the detailed role of FSCN1 in gastric cancer remains to be elucidated. In the present study, downregulation of microRNA (miR)-133a and upregulation of FSCN1 were both observed in gastric cancer tissues and cell lines. Functional studies have revealed that miR-133a is able to bind to the 3'-untranslated region of FSCN1 mRNA, and overexpression of miR-133a causes downregulation of FSCN1 expression, while downregulation of miR-133a leads to an increased FSCN1 expression in gastric cancer cells. Furthermore, overexpression of miR-133a inhibited proliferation and invasion, but promoted apoptosis of gastric cancer cells, which may be reversed by upregulation of FSCN1. By contrast, downregulation of miR-133a enhanced proliferation and invasion, but suppressed apoptosis in gastric cancer cells. In conclusion, the anti-oncogenic activity of miR-133a may involve the inhibition of the target gene FSCN1. The present study suggested that miR-133a may be a potential therapeutic target in the treatment of gastric cancer. 

Retracted: Yes

PubPeer comments:
 *[above]* Fig 4C.  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] Several panels are shared across two otherwise-unrelated papers. How to explain the coincidence? , 
 #1 Now with some additional mark-up: ![file] Highlighting similarity to panels of Figs 2(C) and 4(C) of [Jiao et al (2016)] . ![file] , 
 *[below[* Fig 4B.  ... 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. *[above]* Fig 4A from [Peng et al (2013)] .  Flow cytometry was used to determine the apoptotic rate of U87 and CHG-5 cells after forced downregulation of RACK1.  ![file] Two pairs of hockey sticks are unexpectedly similar. UPDATE: More coloured rectangles added, to bring Figs 2C; 4B of [He et al (2015)] into the mix. ![file] Figs 1C, 4D from [Zhao et al (2015)] .  Overexpression of miR-148a promoted paclitaxel-induced cell apoptosis, whereas inhibition of miR-148a suppressed paclitaxel-induced cell apoptosis, compared with the control group ;  Overexpression of PDIA3 inhibited paclitaxel-induced cell apoptosis, whereas inhibition of PDIA3 promoted paclitaxel-induced cell apoptosis, compared with the control . ![file] , 
 Retracted [1 June 2021] . ---------------------------------------------------- Following the publication of this paper, it was drawn to the Editorsu2019 attention by a concerned reader that certain of the flow cytometric data in the article (featured in Fig. 4B) were strikingly similar to data that had appeared in different form in another article by different authors. Owing to the fact that the contentious data in the above article had already appeared in different form in another article prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. -------------------------------------------- Background [here] . ,