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PurposeMerkel cell carcinoma (MCC) is a highly malignant cancer associated with dismal survival outcomes. Surgery is the cornerstone for the management of MCC, but the benefit of radiotherapy (RT) and chemotherapy (CT) is still controversial. We aimed to investigate the prognostic value of RT and CT in the management of stage I-III MCC patients using the Surveillance, Epidemiology, and End Results (SEER) database.MethodsPatients with a histopathological diagnosis of MCC between 2010 and 2016 were included. The primary endpoint of this study was overall survival (OS). The prognostic significance for OS was analyzed by Cox proportional hazard regression model.ResultsA total of 1,691 patients were identified in the SEER database. Over half of the patients had received RT (56.7%), and 9.8% of the patients were documented to have received CT. The median OS for the entire cohort was 66.0 months, and the 5-year OS rate was 53.8%. In the multivariate analysis, receiving RT was associated with significantly improved OS (P < 0.001), while receiving CT significantly negatively impacted OS (P = 0.010). In stage III patients who underwent treatment based on surgical resection, RT was still demonstrated to be a positive factor (P = 0.002), while CT had no significant association with OS in the univariate analysis (P = 0.295).ConclusionsThe current data in the SEER database are consistent with earlier studies supporting the benefit of adjuvant RT for stage I-III MCC patients, but caution should be taken regarding the routine use of CT. For stage III MCC patients, the value of adjuvant CT needs to be confirmed in future studies.

AbstactConventional therapies and novel molecular targeted therapies against breast cancer have gained great advances over the past two decades. However, poor prognosis and low survival rate are far from expectation for improvement, particularly in patients with triple negative breast cancer (TNBC). Here, we found that lncRNA DANCR was significantly overregulated in TNBC tissues and cell lines compared with normal breast tissues or other type of breast cancer. Knockdown of DANCR suppressed TNBC proliferation both in vitro and in vivo. Further study of underlying mechanisms demonstrated that DANCR bound with RXRA and increased its serine 49/78 phosphorylation via GSK3β, resulting in activating PIK3CA transcription, and subsequently enhanced PI3K/AKT signaling and TNBC tumorigenesis. Taken together, Our findings identified DANCR as an pro-oncogene and uncoverd a new working pattern of lncRNA to mediate TNBC tumorigenesis, which may be a potential therapeutic target for improving treatment of TNBC.

Nicotine has been found to induce the proliferation of lung cancer cells through tumor invasion and to confer resistance to apoptosis. Periostin is abnormally highly expressed in lung cancer and is correlated with angiogenesis, invasion and metastasis. Here, we investigated the roles of periostin in the lung cancer cell proliferation, drug resistance, invasion and epithelial-mesenchymal transition (EMT) induced by nicotine. The periostin gene was silenced using small interfering RNA (siRNA) in A549 non-small cell lung cancer (NSCLC) cells. The cells were transfected with control or periostin siRNA plasmids. Periostin mRNA was evaluated by quantitative reverse transcription-polymerase chain reaction (RT-PCR). Cell proliferation was detected using the MTT assay and cell apoptosis was detected by Annexin V-FITC and propidium iodide (PI) double staining. Tumor invasion was detected by the Boyden chamber invasion assay. Western blotting was performed to detect the expression of the EMT marker Snail. Our results revealed that stably periostin-silenced cells were acquired by G418 screening, and the periostin mRNA expression levels of which were decreased by nearly 80%. Periostin-silenced A549 cells exhibited reduced cell proliferation, elevated sensitivity to chemotherapy with cisplatin, decreased cell invasion and Snail expression (P

W and Mo co-doped VO2(B) nanobelts which used formic acid as reduction acid, NH4VO3 as vanadium source, (NH4)6W7O24 · 6H2O and (NH4)6Mo7O24 · 4H2O as doped sources were synthesised by the hydrothermal method. The samples were characterised by X-ray diffraction (XRD), scanning electron microscope (SEM), transmission electron microscopy (TEM), Fourier transform infrared (FTIR) and X-ray photoelectron spectroscopy (XPS). TEM and HRTEM images showed the samples had a length of 1 µm and a width of 100 nm. XRD, FTIR and XPS spectra revealed that Mo6+ and W6+ incorporated into the VO2(B) lattice and formed solid-solution phases with VO2(B).

Purpose This study was aimed to identify the expression pattern of vascular endothelial growth factor (VEGF) in non-small cell lung cancer (NSCLC) and to explore its potential correlation with the progression of NSCLC. Methods Gene expression profile GSE39345 was downloaded from the Gene Expression Omnibus database. Twenty healthy controls and 32 NSCLC samples before chemotherapy were analyzed to identify the differentially expressed genes (DEGs). Then pathway enrichment analysis of the DEGs was performed and protein-protein interaction networks were constructed. Particularly, VEGF genes and the VEGF signaling pathway were analyzed. The sub-network was constructed followed by functional enrichment analysis. Results Total 1666 up-regulated and 1542 down-regulated DEGs were identified. The down-regulated DEGs were mainly enriched in the pathways associated with cancer. VEGFA and VEGFB were found to be the initiating factor of VEGF signaling pathway. In addition, in the epidermal growth factor receptor (EGFR), VEGFA and VEGFB associated sub-network, kinase insert domain receptor (KDR), fibronectin 1 (FN1), transforming growth factor beta induced (TGFBI) and proliferating cell nuclear antigen (PCNA) were found to interact with at least two of the three hub genes. The DEGs in this sub-network were mainly enriched in Gene Ontology terms related to cell proliferation. Conclusion EGFR, KDR, FN1, TGFBI and PCNA may interact with VEGFA to play important roles in NSCLC tumorigenesis. These genes and corresponding proteins may have the potential to be used as the targets for either diagnosis or treatment of patients with NSCLC.