miR-202-3p negatively regulates MMP-1 to inhibit the proliferation, migration and invasion of lung adenocarcinoma cells.

Lung adenocarcinoma (LUAD) is one of the common cancers. Studies show that MMP-1 is involved in tumor progression, yet relevant regulatory mechanism in LUAD remains to be further elucidated. Here, we demonstrated from bioinformatics analysis for GEO data that MMP-1 was differentially up-regulated in LUAD.

Effect and mechanism of miR-146a on malignant biological behaviors of lung adenocarcinoma cell line.

The aim of the present study was to assess the expression of microRNA-146a (miR-146a) in human lung adenocarcinoma cells, its effect on cellular behaviors, and the underlying molecular mechanisms. Reverse transcription-quantitative PCR (RT-qPCR) was used to measure miR-146a expression in the human normal lung epithelial cell line, BEAS-2B, and human lung adenocarcinoma cell lines, A549, PC-9 and H1299, to determine whether miR-146a acts as an oncogene or anti-oncogene. miR-146a mimics were transfected into target cells to observe the proliferation, apoptosis, invasion and migration of human lung adenocarcinoma cells.

Antitumor activity of interleukin-18 on A549 human lung cancer cell line.

Objective: In this study, we investigated the antitumor activity of interleukin (IL)-18 on A549 human lung cancer cell line and evaluated the potential of IL-18 therapy in lung cancer.

Materials And Methods: We generated a human IL-18 lentiviral expression vector and examined three groups of A549 cells, including nontransduced cells and cells transduced with either IL-18 or an empty lentiviral expression vector. IL-18 expression, cell proliferation, and apoptosis were examined using Western blotting, methylthiazolyldiphenyl-tetrazolium bromide assay, and flow cytometry, respectively.

Effect of lentiviral vector-packaged interleukin-18 gene on the malignant behavior of lung cancer.

Interleukin-18 (IL-18) is a multifunctional cytokine that exhibits antitumor, anti-infection and immunoregulatory functions. This study aimed to investigate the effects of lentiviral vector-packaged interleukin (IL)-18 gene on the malignant behavior of lung cancer and the potential underlying molecular mechanism of IL-18 anticancer activity. Human lung adenocarcinoma A549 cells transfected with human IL-18 gene-containing lentiviral expression vector were the IL-18 intervention group (group A), cells transfected with the empty lentiviral expression vector were empty vector group (group B), and cells without any intervention were the blank control group (group C).

IL‑21/IL‑21R inhibit tumor growth and invasion in non‑small cell lung cancer cells via suppressing Wnt/β‑catenin signaling and PD‑L1 expression.

Lung cancer is considered to be one of the world's deadliest diseases, with non‑small cell lung cancer (NSCLC) accounting for 85% of all lung cancer cases. The present study aimed to investigate the role and underlying mechanisms of interleukin‑21 (IL‑21), and its receptor IL‑21R, in NSCLC. Lung tissues and blood samples of NSCLC were used to measure IL‑21, IL‑21R and programmed death 1 ligand 1 (PD‑L1) expression using ELISA, western blot and immunohistochemistry analyses.

Preliminary evaluation of the potential role of β-elemene in reversing erlotinib-resistant human NSCLC A549/ER cells.

β-elemene (β-ELE) is a natural compound extracted from that has shown promise as a novel anticancer drug to treat malignant tumors. Recent studies have demonstrated that β-ELE can reverse the drug resistance of tumor cells. To the best of our knowledge, there are no reports concerning the reversal of erlotinib resistance by β-ELE in human non-small cell lung cancer (NSCLC) cells.

Tripchlorolide induces autophagy in lung cancer cells by inhibiting the PI3K/AKT/mTOR pathway and improves cisplatin sensitivity in A549/DDP cells.

Tripchlorolide (T4) has been shown to induce A549 lung cancer cell death predominantly by activating an autophagy pathway. However, the underlying mechanism remains unclear. Herein, we demonstrated that compared with T4 treatment alone, pretreatment with wortmannin (an inhibitor of phosphatidylinositol 3-kinase), perifosine (an inhibitor of AKT) or rapamycin (an inhibitor of mTOR) combined with a subsequent T4 treatment significantly impaired the cell viability of A549 and A549/DDP lung cancer cells.

Primary lymphoepithelioma-like carcinoma of the lung: An unusual cancer and clinical outcomes of 14 patients.

Advanced lung cancer is considered to exhibit a poor prognosis; however, the pulmonary lymphoepithelioma-like carcinoma (LELC), a rare subtype of non-small cell lung cancer (NSCLC), exhibits an improved prognosis, compared with non-LELC. The present study aimed at investigating the clinical manifestation, imaging characteristics, pathology, tumor markers, treatment and prognosis of primary LELC of the lung. A total of 14 patients with pulmonary LELC were confirmed by surgery and pathology.

Clinicopathological significance of oestrogen receptor expression in non-small cell lung cancer.

Objective To investigate the expression and clinicopathological significance of the oestrogen receptor (ER) in non-small cell lung cancer (NSCLC). Methods ER expression was examined by immunohistochemical staining of tumour tissue and adjacent normal lung tissue from 67 NSCLC patients. The relationships between ER expression and clinicopathological features were analysed.

[The efficacy and safety of moxifloxacin in the treatment of patients with acute exacerbation of chronic obstructive pulmonary disease].

Objective: To compare the effectiveness and safety of moxifloxacin and cefoperazone-sulbactam therapy in acute exacerbation of chronic obstructive pulmonary disease (COPD).

Methods: This was a prospective, randomized, multicentre study conducted between December 2011 and December 2012 involving 21 hospitals in Fujian. A total of 202 patients with AECOPD requiring antibiotic therapy were enrolled.

Effects and mechanism of downregulation of survivin expression by RNA interference on proliferation and apoptosis of lung cancer cells.

The survivin protein, a member of the inhibitors of apoptosis (IAP) family, has gained popularity as a therapeutic target for cancer due to its selective expression in tumor cells and its significant involvement in tumor cell viability. The aim of this study was to investigate the effect of the survivin-small interfering RNA (siRNA) plasmid on survivin expression in the human lung cancer cell line, A549, and to observe its effects on apoptosis and proliferation of A549 cells. A549 human lung cancer cells were transfected with survivin-targeting siRNA.

Tripchlorolide induces cell death in lung cancer cells by autophagy.

It has been demonstrated that triptolide inhibits the growth of several types of cancer cells in vitro and prevents tumor growth in vivo by inducing apoptosis and autophagy. Here we showed that Tripchlorolide (T4) significantly suppressed the proliferation of A549 cells in a dose- and time-dependent manner. This suppressive effect was diminished when cells were pretreated with 3-Methylamphetamine (3-MA).

[Clinical features of 127 cases of novel influenza A (H1N1) infection in Fujian Province].

Objective: to investigate the clinical features of 127 cases of the novel influenza A/H1N1 infection in Fujian Province.

Methods: this study included 127 human cases with the novel influenza A/H1N1 infection in Fujian Province from May 2009 to July 2009. Data were collected and reviewed from hospital medical records.

[Effects of interleukin-18 on asthmatic airway inflammation: experimental study of guinea pig asthmatic model].

Objective: To investigate the effects of Interleukin-18 (IL-18) on asthmatic airway inflammation.

Methods: Thirty healthy adult male guinea pigs were randomly divided into 3 equal groups: asthmatic model group (Group A, undergoing intraperitoneally injection of ovalbumin (OVA) once and spraying of OVA aerosol once a day for 5 days; control group (Group B), undergoing intraperitoneally injection of OVA once and spraying of normal saline aerosol once a day for 5 days; and interleukin (IL)-18 intervention group (Group C, undergoing intraperitoneally injection of OVA once and intraperitoneal injection of IL-18 on the days 1, 3, 8. 10.