The aim was to investigate the clinicopathological characteristics, diagnosis, and prognosis of sarcomatoid carcinoma of the lung. We reviewed 114 cases of sarcomatoid carcinoma of the lung in patients that were admitted to the First Affiliated Hospital of Zhengzhou University and Anyang Tumor Hospital from January 2009 to March 2018. We analyzed the clinical characteristics, immunohistochemical profiles, treatments, and overall survival of the patients. The patient population included 88 men and 26 women. Median patient age was 65 years (range 37-88 years), and the gender ratio (M/F) was 3.4:1. Median survival was 3.5 months (range 0.5-60 months). Univariate analysis showed that tumor location, tumor size, M stage, TNM stage, chemotherapy, and surgery were all prognostic factors for survival (P < 0.05). We found that T stage, surgery, and chemotherapy were independent prognostic factors for sarcomatoid carcinoma (P < 0.05). Pulmonary sarcomatoid carcinoma is a rare tumor with a poor prognosis. Patients with smaller T stage, complete resection, and chemotherapy exhibited a better prognosis. Early diagnosis and early treatment are important to improve the prognosis of these patients.

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BackgroundBostrycin is a novel compound isolated from marine fungi that inhibits proliferation of many cancer cells. However, the inhibitory effect of bostrycin on lung cancers has not been reported. This study is to investigate the inhibitory effects and mechanism of bostrycin on human lung cancer cells in vitro.MethodsWe used MTT assay, flow cytometry, microarray, real time PCR, and Western blotting to detect the effect of bostrycin on A549 human pulmonary adenocarcinoma cells.ResultsWe showed a significant inhibition of cell proliferation and induction of apoptosis in bostrycin-treated lung adenocarcinoma cells. Bostrycin treatment caused cell cycle arrest in the G0/G1 phase. We also found the upregulation of microRNA-638 and microRNA-923 in bostrycin-treated cells. further, we found the downregulation of p110α and p-Akt/PKB proteins and increased activity of p27 protein after bostrycin treatment in A549 cells.ConclusionsOur study indicated that bostrycin had a significant inhibitory effect on proliferation of A549 cells. It is possible that upregulation of microRNA-638 and microRNA-923 and downregulaton of the PI3K/AKT pathway proteins played a role in induction of cell cycle arrest and apoptosis in bostrycin-treated cells.

BackgroundMacrophage migration inhibitory factor (MIF) is important in regulating cell proliferation and apoptosis in both normal and cancerous cells, and may be important in cancer progression and metastasis. In human non-small cell lung cancer (NSCLC), the underlying mechanisms responsible for MIF-dependent regulation of cellular proliferation, and cell death remain poorly appreciated.MethodsThe human H460 lung cancer cell-line was treated with an optimally determined dose of 50 pmol/ml MIF siRNA, following which cell proliferation, cell cycle and apoptosis were analyzed. Additionally, known pathways of apoptosis including expression of Annexin-V, enhanced production of caspases-3 and −4 and expression of the Akt signaling protein were assessed in an attempt to provide insights into the signaling pathways involved in apoptosis following disruption of MIF expression.ResultsSpecific siRNA sequences markedly decreased MIF expression in H460 cells by 2 to 5-fold as compared with the negative control. Moreover, MIF miRNA dampened not only cellular proliferation, but increased the frequency of apoptotic cells as assessed by cell-surface Annexin-V expression. Entry of cells into apoptosis was partly dependent on enhanced production of caspases −3 and −4 while not affecting the expression of either caspase-8 or the Akt signaling pathway.ConclusionsIn a model of NSCLC, knockdown of MIF mRNA expression dampened H460 proliferation by mechanisms partly dependent on entry of cells into apoptosis and enhanced production of caspase-3 and −4. MIF expression may thus be important in NSCLC progression. Targeting MIF may have clinical utility in the management of human lung cancer.

Adjuvant chemotherapy has been established as standard treatment for advanced cancer among multidisciplinary therapies. A simple and instructive biomarker for therapeutic response and recurrence is needed to evaluate the therapeutic effect. Jab1/COPS5 level has been shown to be associated with tumor progression and poor outcomes in many types of cancer patients. This study aims to further evaluate the clinical and prognostic value of Jab1/COPS5 level as a biomarker in lung and breast cancer patients receiving adjuvant chemotherapy. In this study, data of 88 lung cancer and 76 breast cancer patients were retrospectively collected and analyzed to identify the relationship between the Jab1/COPS5 level and the clinical progression and outcome of these patients. Lung cancer patients with increased Jab1/COPS5 level tend to be non-responsive to chemotherapy. Relapsed breast cancer patients had an increased Jab1/COPS5 level and breast cancer patients with increased Jab1/COPS5 level had significantly shorter disease-free survival and overall survival. In a multivariate survival analysis, histological type and Jab1/COPS5 were associated with disease-free survival and overall survival. The Jab1/COPS5 level was found to be a possible biomarker for clinical response to chemotherapy in lung cancer patients and for postoperative relapse in breast cancer patients who received adjuvant chemotherapy. In conclusion, this study identified Jab1/COPS5 as novel prognostic markers for lung cancer and breast cancer.