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Long noncoding RNA small nucleolar RNA host gene 4 (SNHG4) is usually up-regulated in cancer and regulates the malignant behavior of cancer cells. However, its role in lung cancer remains elusive. In this study, we silenced the expression of SNHG4 in NCI-H1437 and SK-MES-1, two representative non-small-cell lung cancer cell lines, by transfecting them with siRNA (small interfering RNA) that specifically targets SNHG4. We observed significantly inhibited cell proliferation in vitro and reduced tumor growth in vivo after SNHG4 silencing. SNHG4 knockdown also led to cell cycle arrest at the G1 phase, accompanied with down-regulation of cyclin-dependent kinases CDK4 and CDK6. The migration and invasiveness of these two cell lines were remarkably inhibited after SNHG4 silencing. Moreover, our study revealed that the epithelial–mesenchymal transition (EMT) of lung cancer cells was suppressed by SNHG4 silencing, as evidenced by up-regulated E-cadherin and down-regulated SALL4, Twist, and vimentin. In addition, we found that SNHG4 silencing induced up-regulation of miR-98-5p. MiR-98-5p inhibition abrogated the effect of SNHG4 silencing on proliferation and invasion of lung cancer cells. In conclusion, our findings demonstrate that SNHG4 is required by lung cancer cells to maintain malignant phenotype. SNHG4 probably exerts its pro-survival and pro-metastatic effects by sponging anti-tumor miR-98-5p.

Calcium (Ca2+)/calmodulin-dependent protein kinase II (CaMKII) had been reported to play a role in the process of fertilization. However, the role of CaMKII in the release of diplotene-arrested oocytes is poorly understood. In this study, we explored the potential effect of CaMKII on Akt1 and the relationship among CaMKII, Akt1 and phosphatidylinositol (3,4,5)-trisphosphate (PIP3) during the meiotic resumption of mouse oocytes. We found that inhibition of CaMKII aggravated diplotene arrest. We detected the expression and distribution of pCaMKII (Thr286), pAkt1 (Ser473), Cdc25B and pCdc2 (Tyr15) when oocytes were treated with KN-93, SH-6, LY294002 or PIP3, respectively. Our data showed that down-regulated CaMKII by KN-93 decreased the levels of pAkt1 (Ser473) and rearranged the distribution of pAkt1 (Ser473). Meanwhile, down-regulated pAkt1 (Ser473) by SH-6 also decreased the levels of pCaMKII (Thr286), Cdc25B and pCdc2 (Tyr15) significantly and rearranged the distributions of pCaMKII (Thr286). Furthermore, our data showed that exogenous PIP3 up-regulated GVBD rates significantly and increased the levels of pCaMKII (Thr286) and pAkt1 (Ser473). On the contrary, down-regulation of PIP3 by LY294002 decreased GVBD rates and the levels of pCaMKII (Thr286) and pAkt1 (Ser473), respectively. Our results showed that Akt1 and CaMKII regulated each other, and PIP3 may be involved in these regulations during the release of mouse oocytes from diplotene arrest.

Long-term exposure to greenhouse environments exposes greenhouse workers to inhalation of antigens that can cause respiratory diseases. This study was conducted to investigate the prevalence and potential risk factors for bronchial asthma among the Chinese greenhouse workers based on questionnaire and spirometry data. This was an observational cross-sectional study, performed via stratified-cluster-random sampling. It was conducted in Liaoning Province from the northeast of People’s Republic of China, using a population-based sample of 5,880 workers at 835 plastic film greenhouses. All subjects were interviewed using a standardized questionnaire and underwent pulmonary function tests. Multiple logistic regression analysis was conducted to assess associations between self-reported factors of greenhouse worker exposure and bronchial asthma and to identify potential risk factors for this disease. A total of 5,420 questionnaires were completed. The overall prevalence of asthma in greenhouse workers was 19.2% (1040/5420). Multiple logistic regression analysis revealed that the use of multiple pesticides (odds ratio [OR] 1.24, 95% confidence interval [CI] 1.03–1.49), bad odors in the greenhouse (OR = 1.26, 95% CI = 1.07–1.49), and report of the onset of cough when entering the greenhouse (OR = 1.25, 95% CI = 1.09–1.44) were associated with the development of asthma. In contrast, a higher body mass index (BMI >18.5 kg/m2, OR = 0.93, 95% CI = 0.90–0.95), planting flowers (OR = 0.92, 95% CI = 0.87–0.98), open sidewall to outside (natural ventilation) for at least 30 min per event (OR = 0.82, 95% CI = 0.69–0.96), living in greenhouse (OR = 0.85, 95% CI = 0.73–0.99), and experiencing cough before 14 years old (OR = 0.61, 95% CI = 0.43–0.84) were protective factors to the presentation of asthma among greenhouse workers. Our results suggest that asthma is a major public health problem among Chinese greenhouse workers and more attention should be devoted to preventive measures and management of this disease.

Aim To investigate the role of translationally controlled tumor protein (TCTP) in lung cancer development. Main methods A549 and HCC827 cells were transfected with shRNA specifically targeting TCTP mRNA. Cell growth was assessed by colony formation assay and cell counting kit-8. Cell cycle and apoptosis were analyzed by flow cytometry. Cell migration and invasion was measured by scratch and transwell assays. In vivo tumorigenicity was evaluated by tumor xenografts in nude mice. Key findings TCTP -silenced cells displayed a reduced ability of colony formation and a lower rate of proliferation in vitro . Knockdown of TCTP arrested cell cycle at G1 phase and led to downregulated expression of cyclins B1, D1 and E. Moreover, silencing of TCTP induced apoptosis and altered the levels of apoptosis-regulatory proteins such as cleaved caspase-3, Bcl-2, Bax and p53. Silencing of TCTP also inhibited migration and invasion of lung cancer cells. In addition, TCTP -silenced A549 cells, when subcutaneously inoculated in nude mice, formed tumors at a significantly slower rate. Significance Our in vitro and in vivo data indicate that silencing of TCTP inhibits growth, migration and invasion of lung cancer cells. Thus, TCTP may be a potential target for lung cancer therapy.

Integrin-linked kinase (ILK) is a highly conserved serine-threonine protein kinase which has been implicated in the regulation of various cellular processes. Previously, we have demonstrated that overexpression of ILK correlates with malignant phenotype in non-small cell lung cancer. Furthermore, forced overexpression of ILK promotes lung cancer cell invasion and migration. However, the molecular mechanisms by which ILK enhances the invasive phenotype of lung cancer cells are still not fully understood. In the present study, we found that overexpression of ILK stimulated matrix metalloproteinase-9 (MMP-9) expression and activity in lung cancer cells. ILK-induced cell migration and invasion were significantly inhibited by MMP inhibitor doxycycline as well as by anti-MMP-9 neutralizing antibody. In addition, overexpression of ILK induced phosphorylation and nuclear translocation of nuclear factor-κB (NF-κB) subunit p65. Finally, upregulation of MMP-9 was severely abolished by either BAY 11-7028, a specific NF-κB inhibitor, or small interfering RNA targeted to NF-κB p65 in ILK overexpression cells. Taken together, these findings suggest that ILK promotes lung cancer cell migration and invasion via NF-κB-mediated upregulation of MMP-9.

Integrin-linked kinase (ILK), a member of the serine/threonine kinases, has been implicated in oncogenesis and progression of human cancers. The aim of this study was to characterize the role of ILK in lung cancer aggressiveness and the underlying molecular mechanisms. ILK protein expression was assessed by immunohistochemistry in a cohort of non-small cell lung cancer (NSCLC) patients, and a series of in vitro assays was conducted to elucidate the function of ILK in lung cancer. Overexpression of ILK protein was detected in 30.6% (33/108) of primary NSCLC tissues and correlated with the TNM stage (P=0.001) and lymph node metastasis (P=0.033). Ectopic overexpression of ILK in lung cancer cells promoted cell migration and invasion in vitro, and led to the acquisition of epithelial-mesenchymal transition (EMT) phenotype, as evidenced by the spindle-like morphology, down-regulation of E-cadherin, and up-regulation of vimentin, fibronectin, Snail and Slug. In addition, the down-regulation of E-cadherin induced by ILK was significantly reversed by nuclear factor-κB (NF-κB) inhibitor BAY 11-7028 and small interfering RNA (siRNA) targeting NF-κB p65, suggesting a role of the NF-κB signaling pathway in ILK-induced EMT. Overall, our results suggest that ILK promotes lung cancer cell migration and invasion through the induction of EMT process.

With respect to the limited field of view in the visual environment sensory perceptual system of the traditional three-dimensional reconstruction system, as well as such defects as high price, big size, cumbersome shape and low rate of imaging, a three-dimensional reconstruction system is designed based on panoramic vision and a two-dimensional ranging laser. By adopting the linear laser technology, a non-contact hardware system of laser scanning and measuring system is constructed based on panoramic vision, so as to achieve real-time scanning of objects; by adopting the corner detection technology to abstract image features, and to perform image matching and camera calibration, a three-dimensional model of objects is constructed. System software tests developed in the programming environment of Visual C++ show that this system could realize an excellent three-dimensional reconstruction based on panoramic vision and two-dimensional ranging laser.