BackgroundNon-small cell lung cancer (NSCLC) is the leading cause of cancer mortality worldwide. Distant metastasis is thought to be one of the most important factors responsible for the failure of NSCLC therapy. MicroRNA-7-5p (miR-7-5p) has been demonstrated to be a tumor suppressor in breast cancer, hepatocarcinoma, prostate cancer and glioblastoma multiforme (GBM). However, its role in NSCLC is still not fully understood. This study evaluated the role of miR-7-5p in the progression of NSCLC and explored the underlying mechanism.Materials & methodsThe quantitative real-time PCR (qPCR), MTT, migration and invasion assays were used to evaluate the effects of miR-7-5p on the proliferation, migration and invasion of A549 and SPCA-1 cells. A tumor xenograft model was created to determine the effects of miR-7-5p on metastasis in vivo. The dual-luciferase reporter gene, neuro-oncological ventral antigen 2 (NOVA2) overexpression and western blotting assays were performed to explore the underlying mechanism.ResultsMiR-7-5p is downregulated in NSCLC tissues and lung cancer cell lines. It suppresses proliferation, migration, invasion and EMT marker expression in vitro and in vivo. Further study showed that miR-7-5p suppresses tumor metastasis of NSCLC by targeting NOVA2. Overexpression of NOVA2 attenuates the miR-7-5p-mediated inhibitory effect on lung cancer cells.ConclusionMiR-7-5p suppresses NSCLC metastasis. Targeting miR-7-5p may contribute to the success of NSCLC therapy.

Long non-coding RNAs (lncRNAs) are important regulatory factors in tumor development and progression. The lncRNA CASC9.5 is located on chromosome 8 and has a total length of 1316 bp. CASC9.5 plays a tumor-promoting role in the development and progression of brain tumor and colon cancer; however, limited research has been conducted on the role of this lncRNA in lung adenocarcinoma. The present study analyzed 44 lung adenocarcinoma specimens and 2 lung cancer cell lines. It was found that CASC9.5 expression levels were significantly higher in lung cancer tissues and cells compared with normal lung tissues. In addition, the expression level of CASC9.5 was closely related to the TNM (tumor, node and metastasis) stage of lung adenocarcinomas, tumor size, tumor metastasis and tumor metabolism. Moreover, results of the in vivo and in vitro experiments all demonstrated that CASC9.5 promoted lung adenocarcinoma cell proliferation and metabolism by regulating the expression levels of cyclin D1, E-cadherin, N-cadherin and β-catenin. In summary, the present study demonstrated that high levels of CASC9.5 expression promote the proliferation, metastasis and metabolism of lung adenocarcinoma cells and might serve as a prognostic indicator. The present study provides novel findings regarding the diagnosis and treatment of lung adenocarcinoma.

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Background: Extended thymectomy is indicated for patients with myasthenia gravis (MG) when drugresistance or dependence is seen. We have employed a technique for subcostal thoracoscopic extended thymectomy (STET) on patients with MG. Conclusions: This procedure showed satisfactory results for patients with MG. Moreover, the STET approach is more easily for surgeons to fully reveal the bilateral phrenic nerve and the upper thymic poles. We believe that STET is a satisfactory procedure for performing extended thymectomy in well selected patients.