MicroRNA-625 inhibits the progression of non‚Äësmall cell lung cancer by directly targeting HOXB5 and deactivating the Wnt/Œ≤-catenin pathway
Authors: Lihua Jiang
Xia Wu
Qingfang Lin
Xiaoxia Tan
Wen Feng
Journal: International Journal of Molecular Medicine (2019)
Discipline: CLINICAL MEDICINE
Keywords: microRNAs; miR-625; non-small cell lung cancer; NSCLC; expression
Affiliations: Department of Respiratory Disease, The Third People's Hospital of Linyi, Linyi, Shandong 276023, P.R. China., Department of Oncology, The Third People's Hospital of Linyi, Linyi, Shandong 276023, P.R. China., Department of Pediatrics, The Third People's Hospital of Linyi, Linyi, Shandong 276023, P.R. China.

Abstract:  Numerous microRNAs (miRs) are dysregulated in non‚Äësmall cell lung cancer (NSCLC), serving pivotal roles in its formation and progression. miR‚Ä?25 is dysregulated in several types of human cancer, but its involvement in the formation and development of NSCLC remains poorly understood. In the present study, we aimed to investigate miR‚Ä?25 expression in NSCLC and its role in regulating NSCLC cell behavior. miR‚Ä?25 expression in NSCLC tissues and cell lines was detected using reverse transcription‚Äëquantitative polymerase chain reaction. The effects of miR‚Ä?25 overexpression on NSCLC cell proliferation, apoptosis, migration and invasion in vitro were assessed using an MTT assay, flow cytometry, and cell migration and invasion assays, respectively. The effects of miR‚Ä?25 upregulation on NSCLC growth were evaluated in an in vivo xenograft model. The molecular mechanisms underlying the tumor‚Äësuppressing roles of miR‚Ä?25 in NSCLC were explored in detail. miR‚Ä?25 expression was determined to be downregulated in NSCLC tissues and cell lines. This decreased expression was associated with advanced clinical features and poor overall survival of patients with NSCLC. Exogenous miR‚Ä?25 expression suppressed NSCLC cell proliferation, migration and invasion, and induced apoptosis in vitro. miR‚Ä?25 upregulation hindered NSCLC tumor growth in vivo. Homeobox B5 (HOXB5) was proposed to be the direct target gene of miR‚Ä?25 in NSCLC cells. The tumor‚Äësuppressing effects of HOXB5 silencing were similar to those of miR‚Ä?25 overexpression in NSCLC cells. In rescue experiments, HOXB5 overexpression partially reversed the inhibitory effects of miR‚Ä?25 in NSCLC cells. miR‚Ä?25 upregulation directly targeted HOXB5 to deactivate the Wnt/Œ≤‚Äëcatenin signaling pathway in NSCLC cells in vitro and in vivo. miR‚Ä?25 was determined to be associated with HOXB5 suppression and Wnt/Œ≤‚Äëcatenin pathway deactivation, which in turn inhibited the aggressive behavior of NSCLC cells in vitro and in vivo. 

Retracted: Yes

PubPeer comments:
 Figs 2C, 4C, 5C.  The purple box marks a panel that has appeared in at least two other papers: Figs 2C,6F,7D of [Mao et al (2017)] , and Figs 3B,5D of [Shen et al (2018)] .  Here in contexts: Mao et al (2017),  And Shen et al (2018).  There may be other matches. , 
 *[left]* Fig 7A from [Zhang et al (2019)] .  Photograph of tumor xenografts obtained from nude mouse injected with miR-802 mimics- or miR-NC-transfected H460 cells . Rotated through 90 deg to facilitate comparison. *[upper right]* Fig 8A from [Wang, Xiao Zhao (2019)] .  miR-675 mimics or miR-NC were transfected into TPC-1 cells and then injected to nude mice. A representative image of tumor xenografts is shown . *[lower right]* **Fig 7B from [Tan et al (2019)] **.  Representative images of tumor xeno-grafts derived from H460 cells transfected with agomir-625 or agomir-NC .  Two pairs of tumors appear to be the same, seen at slightly different angles (red rectangles). Note also that all three institutions seem to be using a single ruler, with a distinctive stain at the lower right. , 
 Retracted [18 April 2022] .  Following the publication of this paper, it was drawn to the Editors attention by a concerned reader that certain of the flow cytometric data shown in Fig. 2C and the images of tumors shown in Fig. 7B 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 *International Journal of Molecular Medicine*, the Editor has decided that this paper should be retracted from the Journal. Independently of this investigation, the authors also requested a retraction of this article owing to the fact that the manuscript had been published without permission from one of the authors. The Editor apologizes to the readership for any inconvenience caused. ,