• Ortega Quinlan posted an update 6 months, 2 weeks ago

    The clinical data demonstrated that high TMOD1 expression is associated with good pathological status in patients with cervical cancer. Overall, the results of the present study indicated that TMOD1 may act as a tumor suppressor in cervical cancer, whereby its downregulated expression was demonstrated to have direct effects on cell motility and cell proliferation. selleck chemicals These results provide new evidence for the prognostic prediction of cervical cancer, which may serve as a promising therapeutic strategy for patients with cervical cancer. Copyright © 2020, Spandidos Publications.Pancreatic ductal adenocarcinoma (PDAC) remains a major cause of cancer-associated mortality, with poor patient outcome. The present study aimed to identify key candidate genes and investigate the potential molecular mechanisms associated with the progression of PDAC. The GSE46234 dataset was downloaded from the Gene Expression Omnibus database, in order to identify the upregulated differentially expressed genes (DEGs) in PDAC. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to determine the biological functions and pathways of the upregulated DEGs, and a protein-protein interaction (PPI) network was subsequently constructed to screen the hub genes. Subsequently, survival analyses of the hub genes were undertaken in patients with PDAC, using The Cancer Genome Atlas dataset. Reverse transcription-quantitative (RT-q)PCR analysis was performed to assess the mRNA expression levels of the hub genes associated with the prognosis of patients with PDAC. In the present stuapeutic targets for PDAC. Copyright © Tian et al.It has been found that >90% of oral cancer patients suffer from squamous cell carcinoma (SCC). The 5-year survival rate of SCC is ~50%, despite the availability of different treatments. Sonodynamic therapy (SDT) has been developed as a novel therapy for cancer, resisting bacterial infection and inhibiting atherosclerotic plaque progression. The present study investigated the efficacy of hematoporphyrin monomethyl ether (HMME)-mediated SDT on the A-253 epidermoid cancer cell line. The cytotoxicity of HMME and the survival rate of cells following SDT were examined by the MTT assay. Apoptosis and necrosis of cells were detected using flow cytometry with Annexin V and propidium iodide (PI) staining, and fluorescence microscopy with Hoechst 33258 and PI staining. Intracellular reactive oxygen species (ROS) and Ca2+ levels were measured using a fluorescence microscope based on 2′,7′-dichlorofluorescein diacetate and fluo-3/acetoxymethylester, respectively. Results of the MTT assay demonstrated that a lower concentrts with SCC. Copyright © Zhang et al.The aim of the present study was to determine the mechanism by which advanced glycation end products (AGEs) induce proliferation, invasion and epithelial-mesenchymal transition (EMT) of human colon cancer SW480 cells. SW480 cells were divided into groups as follows i) Control; ii) cells treated with AGEs alone; and iii) cells treated with AGEs combined with LY294002. Proliferation, cell cycle progression, apoptosis, invasion and migration of SW480 cells were assessed using an MTT assay, flow cytometry, Transwell assays and a wound healing assay, respectively. The protein expression levels of PI3K, AKT and epithelial cadherin (E-cadherin) were examined by western blot analysis in SW480 cells treated with various concentrations of AGEs. Proliferation, invasion and migration were enhanced, cell cycle progression was increased and apoptosis was decreased in SW480 cells treated with AGEs compared with the control. The PI3K inhibitor, LY294002, reversed the effects of AGEs. Western blot analysis data demonstrated that AGEs increased the protein expression levels of PI3K and AKT, and decreased the expression of E-cadherin. The results suggested that AGEs exert a positive effect on the proliferation, invasion and EMT in SW480 cells through the PI3K/AKT signaling pathway. Copyright © Liang et al.Disrupted centrosome-associated family protein expression can result in the detrimental duplication of centrosomes, causing genomic instability and subsequent carcinogenesis. Limited research has demonstrated that centrosomal protein 131 (CEP131) exhibits oncogenic activity in osteosarcoma, hepatocellular carcinoma and breast cancer. The present study demonstrated that there is an association between CEP131 expression and advanced Tumor-Node-Metastasis stage (P=0.016), and positive regional lymph node metastasis (P=0.023) in 91 cases of non-small cell lung cancer. A549 and SPC-A-1 cells, with moderate expression levels of CEP131, were selected as representative cell lines. The results indicated that downregulation of CEP131 induced G1/S cell cycle arrest, inhibition of cyclins D1/E and cyclin-dependent kinases 2/4/6, and induction of inhibitory p21/p27, all of which are regulated by ERK and AKT signaling, suggesting that CEP131 exhibits potential as a novel target in the treatment of lung cancer. Copyright © Wang et al.Malignant spinal cord compression (MSCC) is a serious complication of cancers. The present study aimed to establish a multidisciplinary treatment system for urgent magnetic resonance imaging (MRI) and referral to orthopedists in order to prevent neurological deficits caused by MSCC. In the present study, the extent to which this system achieved early diagnosis and treatment and prevented MSCC-caused neurological deficits was examined. The records from patients with neurological deficits caused by MSCC before (between April 2007 and March 2012; group A) and after (between April 2012 and March 2017; group B) the establishment of the multidisciplinary system at the Shikoku Cancer Center (Ehime, Japan) were retrospectively evaluated. The numbers of patients with neurological deficits were 38 and 7 in groups A and B, respectively. All patients received radiotherapy. The incidence of neurological deficits was 13.2 and 3.4% in groups A and B, respectively (P less then 0.001). The proportion of patients with improvement in the severity of neurological deficits was 5.3 and 28.6% in groups A and B, respectively (P less then 0.001). The interval between physicians’ recognition of a neurological deficit and MRI and the start of treatment, the number of cases, and the severity of neurological deficits were evaluated in groups A and B. The median interval between recognition of a neurological deficit by physicians and MRI was 3 and 0 days in groups A and B, respectively (P less then 0.001). The median interval between physicians’ recognition of a neurological deficit and the start of treatment was 3 and 0 days in groups A and B, respectively (P less then 0.001). By using a multidisciplinary treatment system, the incidence and severity of neurological deficits following treatment were significantly improved. Therefore, the multidisciplinary treatment system used in the present study may be useful for early diagnosis, treatment and prevention of MSCC in patients with bone metastases. Copyright © Nakata et al.

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