Erratum: MicroRNA-137 inhibits cell migration and invasion by targeting bone morphogenetic protein-7 (BMP7) in non-small cell lung cancer cells.

[This corrects the article on p. 10847 in vol. 8, PMID: 26617798.].

In silico insight into EGFR treatment in patients with lung carcinoma and T790M mutations.

The T790M mutational basis of treatment failure, following treatment via alteration of the epidermal growth factor receptor (EGFR) pathway, is a well-known anomaly in patients with non-small cell lung cancer (NSCLC). The T790M mutation activates the kinase domain, causing tyrosine kinase inhibitors, such as gefitinib, to elicit little or no response. To overcome this acquired resistance in NSCLC cells, the present study utilized a structure-based drug designing method to identify a novel lead compound. An in-house traditional Chinese medicinal compound database was used and following initial virtual screening, pre-absorption, distribution, metabolism and excretion/Tox and automated docking analyses, nardosinon was selected as the most appropriate candidate for further analysis. Two NSCLC cell lines, PC9GR4 and H2347, were used to test nardosinon and the results were compared with gefitinib. Results from an initial cell death assay revealed that nardosinon was able to induce cell death in NSCLC cells with and without the T790M mutation. These findings suggest that nardosinon may be an effective pharmacological compound for NSCLC treatment, including T790M EGFR mutant NSCLC cells.

MicroRNA-137 inhibits cell migration and invasion by targeting bone morphogenetic protein-7 (BMP7) in non-small cell lung cancer cells.

MicroRNA-137 (miR-137) was reported to be dysregulated in several human cancers. However, the function and mechanism of miR-137 in non-small cell lung cancer (NSCLC) is still unclear. In the current study, we explored the role of miR-137 in NSCLC progression. Using qRT-PCR, our data showed that miR-137 was significantly down-regulated in NSCLC tissues and cell lines. In vitro functional assay, we found that over-expression of miR-137 suppressed NSCLC cells proliferation, migration and invasion, indicating that miR-137 could act as a tumor suppressor in NSCLC progression. In addition, bone morphogenetic protein-7 (BMP7) was identified as a target of miR-137 in NSCLC cells, Luciferase reporter assay suggested that miR-137 directly targeted 3'-UTR of BMP7, and correlation analysis revealed that BMP7 inversely correlated with miR-137 in NSCLC tissues. Furthermore, Restoration of BMP7 remarkably reversed the tumor suppressive effects of miR-137 on NSCLC cell proliferation, migration, and invasion. Taken together, our findings suggested that miR-137/BMP7 axis could contribute to the progression of NSCLC, suggesting miR-137 as a potential therapeutic target for the treatment of NSCLC.

Increased expression of the lncRNA PVT1 promotes tumorigenesis in non-small cell lung cancer.

INTRODUCTION: Non-small cell lung cancer (NSCLC) is the major cause of cancer death worldwide. Increasing evidence shows that long non coding RNAs (lncRNAs) are widely involved in the development and progression of NSCLC. lncRNA PVT1 in several cancers has been studied, its role in lung cancer remains unknown. Our studies were designed to investigate the expression, biological role and clinical significance of PVT1 in lung cancer. METHODS: lncRNA PVT1 expression in 82 NSCLC tissues and 3 lung cancer cell lines was measured by quantitative Real-time PCR (qRT-PCR). Its association with overall survival of patients was analyzed by statistical analysis. RNA interference (RNAi) approaches were used to investigate the biological functions of PVT1. The effect of PVT1 on proliferation was evaluated by MTT, cell migration and invasion ability was evaluated by cell migration and invasion assays. RESULTS: lncRNA PVT1 expression was significantly upregulated in NSCLC tissues and lung cancer cells when compared with corresponding adjacent normal tissues and normal bronchial epithelial cells. Increased PVT1 expression was significantly correlated with histological grade and lymph node metastasis. In addition, NSCLC patients with PVT1 higher expression have shown significantly poorer overall survival than those with lower PVT1 expression. And PVT1 expression was an independent prognostic marker of overall survival in a multivariate analysis. In vitro assays our results indicated that knockdown of PVT1 inhibited cell proliferation, migration, and invasion. CONCLUSIONS: Our data indicated that lncRNA PVT1 is significantly upregulated in NSCLC tissues and may represent a new biomarker and a potential therapeutic target for NSCLC intervention.