[Retracted] MicroRNA­454 inhibits non­small cell lung cancer cells growth and metastasis via targeting signal transducer and activator of transcription­3.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the cell migration and invasion assay data shown in Figs. 2C and 4D 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 a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 3979­3986, 2018; DOI: 10.3892/mmr.2017.8350].

Apatinib inhibits macrophage-mediated epithelial-mesenchymal transition in lung cancer.

Chemotherapy is one of the main treatment approaches for lung cancer. However, few drugs can be used in the post-first-line treatment of lung cancer. Apatinib is a small molecule inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2) and is widely used in advanced gastric cancer. This study aimed to investigate the therapeutic effect of apatinib in the second-line treatment of lung cancer and explore its underlying mechanism from the aspect of macrophage-mediated epithelial-mesenchymal transition (EMT). The results showed that apatinib attenuated macrophage-induced EMT and migration of lung cancer cells but not normal lung cells, as demonstrated by the loss of epithelial properties and gain of mesenchymal characteristics. Moreover, apatinib selectively decreased hepatocyte growth factor (HGF) secretion in polarized macrophages. Furthermore, apatinib down-regulated the expression of the HGF-Met signaling pathway in polarized macrophage-stimulated lung cancer cells. Taken together, our study has identified a novel pathway through which apatinib exerts its anti-cancer functions, and provided a molecular basis for apatinib potential applications in the post-first line treatment of lung cancer.

MicroRNA-454 inhibits non­small cell lung cancer cells growth and metastasis via targeting signal transducer and activator of transcription-3.

Lung cancer is one of the most common type of cancers and the leading cause of cancer­related mortality worldwide. Non-small cell lung cancer (NSCLC) accounts for >80% of lung cancer cases. Emerging studies have suggested that microRNAs are dysregulated in NSCLC and serve important roles in NSCLC initiation and development. However, to the best of our knowledge, the expression, roles and molecular mechanism of microRNA­454 (miR­454) have not been investigated in NSCLC. In the present study, miR­454 was demonstrated to be significantly downregulated in NSCLC tissues and cell lines, as assessed by western blot analysis and reverse transcription­quantitative polymerase chain reaction. Reduced miR­454 expression was significantly correlated with aggressive clinicopathological features in NSCLC. In addition, upregulation of miR­454 suppressed proliferation, migration and invasion NSCLC cells, as assessed by Cell Counting Kit­8 and in vitro migration and invasion assays, respectively. Furthermore, bioinformatics analysis identified STAT3 as a direct target gene of miR­454, and STAT3 knockdown was demonstrated to simulate the effects of miR­454 overexpression in NSCLC. In conclusion, the present study provided convincing evidence that miR­454 is downregulated in NSCLC, and regulates growth and metastasis by directly targeting STAT3, which suggests that miR­454 may be an efficient therapeutic target for NSCLC.

Drug resistance analysis of gefitinib-targeted therapy in non-small cell lung cancer.

The aim of the study was to examine the drug resistance analysis of gefitinib-targeted therapy in non-small cell lung cancer (NSCLC). In total, 156 NSCLC patients without surgical treatment were selected, including 117 cases of adenocarcinoma (75%), to receive single gefitinib 0.25 g/day or combined with platinum chemotherapy. Computed tomography was used to evaluate tumor growth for the response and non-response groups. The chemotherapy regimen was changed or combined with radiotherapy in the non-response group. Tumor progression or metastasis in the response group was considered as the generation of drug resistance. The chemotherapy regimen was altered in the response group. Eleven cases had tumor response in the non-response group after the chemotherapy regimen was adjusted (20%), 33 cases had complete response (CR) (32.7%), 44 cases had partial response (PR) (43.6%), and 24 cases had stable disease (SD) (23.8%) in the response group. The drug resistance rates of CR, PR, and SD showed no significant difference (P>0.05). However, the drug-resistant time of CR was significantly delayed and the difference was statistically significant (P<0.05). The response rates of CR, PR, and SD patients regaining the response rate showed no statistical significance after the chemotherapy regimen was adjusted, and the difference was not statistically significant (P>0.05). In conclusion, gefitinib-targeted therapy in NSCLC showed certain drug resistance, which may not be related to the response.