[Retracted] MicroRNA­616 promotes the growth and metastasis of non­small cell lung cancer by targeting SOX7.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the cell formation assay data shown in Figs. 3D, 4D, 8D and 9D were strikingly similar to data that had already appeared in another article written by different authors at different research institutes [Wang Z, Jiang C, Chen W, Zhang G, Luo D, Cao Y Wu J, Ding Y and Liu B: Baicalein induces apoptosis and autophagy via endoplasmic reticulum stress in hepatocellular carcinoma. Biomed Res Int: 732516, 2014]. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Oncology 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 a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 38: 2078­2086, 2017; DOI: 10.3892/or.2017.5854].

MicroRNA-616 promotes the growth and metastasis of non-small cell lung cancer by targeting SOX7.

MicroRNAs (miRNAs) are a group of important regulators in human types of cancer including non-small cell lung cancer (NSCLC). miR-616 has been found to be a novel cancer-related miRNA. However, the expression and biological function of miR-616 in NSCLC have not been investigated. In this study, qRT-PCR was performed to evaluate the level of miR-616 in NSCLC tissues. MTT, BrdU and Transwell assay were used to investigate the proliferation and metastasis ability of NSCLC cells. Subcutaneous injection model and tail vein injection model were used to evaluate the effect of miR-616 on the in vivo growth and metastasis of NSCLC cells. It was also found that the expression level of miR-616 was increased in NSCLC tissues and cell lines. Patients with a high level of miR-616 had a significantly shorter overall survival and disease-free survival. Functionally, miR-616 overexpression promoted while miR-616 knockdown inhibited the proliferation, migration and invasion of NSCLC cells. Moreover, miR-616 overexpression enhanced the subcutaneous growth and lung metastasis of NSCLC cells in nude mice. Mechanistically, SOX7 was confirmed to be the downstream target of miR-616 in NSCLC cells. Forced expression of SOX7 prevented the promoting effects of miR-616 overexpression on the proliferation and metastasis of NSCLC cells, while knockdown of SOX7 reversed the inhibitory effects of miR-616 knockdown on the proliferation and metastasis of NSCLC cells. In conclusion, the present study indicates that miR-616 is a promising biomarker and therapeutic target in NSCLC.

Ischemia postconditioning preventing lung ischemia-reperfusion injury.

OBJECTIVE: This study evaluates the inhibitory effect of IPO against ischemia reperfusion (I/R) induced lung injury in rats. METHODS: Anesthetized and mechanically ventilated adult Sprague-Dawley rats were randomly assigned to one of the following groups (n=12 each): the sham operated control group, the ischemia-reperfusion (IR) group (30min of left-lung ischemia and 24h of reperfusion), the IPO group (three successive cycles of 30-s reperfusion per 30-s occlusion before restoring full perfusion), and the dexamethasone plus IPO group (rats were injected with dexamethasone (3mg/kg·day(-1)) 10min prior to the experiment and the rest of the procedures were the same as the IPO group). Lung injury was assessed by wet-to-dry lung weight ratio and tissue apoptosis and biochemical changes. RESULTS: Lung ischemia-reperfusion increased lung MDA production, serum proinflammatory cytokine count, and MPO activity and reduced antioxidant enzyme activities (all p<0.05 I/R versus sham), accompanied with a compensatory increase in caspase-3, bax, Fas, FasL proteins and a decrease in Bcl-2 protein. Plasma levels of TNF-α, IL-6, and IL-1ß were increased in the I/R group (all p<0.05 versus sham). IPO attenuated or prevented all the above changes. Treatment with dexamethasone enhanced all the protective effects of postconditioning. CONCLUSION: Postconditioning obviously inhibits I/R induced lung injury by its antioxidant, anti-inflammatory and anti-apoptosis activities.