Retracted: microRNA‐145‐3p inhibits non‐small cell lung cancer cell migration and invasion by targeting PDK1 via the mTOR signaling pathway
Authors: A-Juan Zheng
Le-Le Wang
Ping Han
Jing Cai
Hong-Bo Ji
Gui-Min Chen
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: PDK1; mTOR pathway; microRNA-145-3p; non-small cell lung cancer.
Affiliations: Department of OncologyLinyi Cancer HospitalLinyiP. R. China, Department of ImagingLinyi People's HospitalLinyiP. R. China, Department of NeurosurgeryLinyi People's HospitalLinyiP. R. China, Department of Respiratory MedicineLinyi People's HospitalLinyiP. R. China, Department of Medical Oncology in Section OneInner Mongolia Chifeng HospitalChifengP. R. China

Abstract:  The mammalian target of rapamycin (mTOR) pathway is dysregulated in more than 50% of all human malignancies and is a major target in cancer treatment. In this study, we explored the underlying mechanism involving microRNA-145-3p (miR-145-3p) in the development and progression of non-small cell lung cancer (NSCLC) by targeting PDK1 via the mTOR signaling pathway. NSCLC tissues and adjacent normal tissues were obtained from 83 NSCLC patients. miR-145-3p, PDK1, and mTOR levels were determined by quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry. Human NSCLC cell lines A549 and H1299 were transfected with miR-145-3p and siPDK1 to confirm the effect of miR-145-3p and PDK1 on NSCLC cells in vitro. Cell growth was evaluated by a CCK8 assay. Cell motility and chemotaxis analysis were determined by the scratch test and chemotaxis assay, respectively. The protein levels of PDK1 and mTOR were measured using the western blotting. Results showed lower level of miR-145-3p and higher levels of PDK1 and mTOR in NSCLC tissues compared to the adjacent normal tissues. In vitro results showed that cell growth, cell motility, and chemotaxis were all inhibited in cells transfected with miR-145-3p and those transfected with siPDK. Additionally, dual luciferase reporter gene assay helped confirmed that PDK1 is a target of miR-145. Finally, levels of PDK1, mTOR, and phosphorylated-mTOR were lower in cells transfected with miR-145-3p as well as those with siPDK1. These findings indicate that miR-145-3p may inhibit cell growth, motility, and chemotaxis in NSCLC by targeting PDK1 through suppressing the mTOR pathway. 

Retracted: Yes

PubPeer comments:
 Fig 7 A,D. ![file] The protein blobs seem to come from the same restricted gamut shown in this montage. The bubble under one of the blobs in a loading control is particularly distinctive. ![] , 
 At right, Fig 2A.  The protein expressions of PDK1 and mTOR in NSCLC and adjacent normal tissues detected by immunohistochemistry Note: A, immunohistochemistry results of PDK1 and mTOR in NSCLC and adjacent normal tissues . At left, Fig. 1A from [Yang et al (2018)] .  Immunohistochemistry results reveal a higher positive rate of MTA1 protein expression in NSCLC tissues (A, u00d7 200). Note: NSCLC, non-small cell lung cancer . ![file] Some uncertainty of identification. Unrelated teams of authors. , 
 #2 Another appearance! Fig 8A from [Song et al (2017)] . ![] , 
 Retracted [30 June 2021] . ----------------------------------------------- The above article, published online on 29 June 2017 in Wiley Online Library has been retracted by agreement between the the journal s Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. A detailed investigation revealed that several image elements of the experimental data were published elsewhere in a different scientific context. Thus, the editors consider the conclusions of this article to be invalid. ,