Friday, 22. 4. 2017    

Cancer Cell Research (Online ISSN: 2161-2609)


Current Issue

Vol.4  No.14


Article: Effects of RNA interference of the eno1 gene on the malignant biological behaviors of gastric cell lines
by  Tingting Chen, Yangqi Liu, Bode Lin, Rongwei He, Zhigang Huang
Cancer Cell Research 2017 4(14) 326-333; published online 27 April 2017
Abstract: To observe the expression of α-Enolase( ENO1) correlated with the pathological progression of gastric cancer and to investigate the effects of ENO1 down-regulation on the proliferative and migratory abilities of gastric cell lines in vitro. The expression of ENO1 was detected in 22 cases of gastric cancer, 20 cases of atypical hyperplasia and 18 cases of normal gastric tissues by immunohistochemistry. The expression level of ENO1 mRNA and protein was determined in AGS cell lines by quantitative real-time reverse transcription PCR (qRT-PCR) and Western blot, respectively. The effects of down-regulation of ENO1 on proliferative and migratory abilities of AGS cells were detected by the experiments of CCK-8, colony formation and wound healing assays. The expression level of ENO1 protein in gastric cancer tissues was higher than that of normal gastric tissues and atypical hyperplasia in the immunohistoehemical study (HC =22.70, P<0.05). It was shown from the cell proliferation curves that the proliferative ability of AGS-ENO1-siRNA transfected group was slower than that of the AGS-NC-siRNA over 72 h (t=2.50, P=0.03), meanwhile, the number of the cell-colonies of the AGS-ENO1-siRNA group were less than that of the control group after 10 days (t=22.05, P =0.01). For the abilitiy of migration, it was significantly decreased in the down-regulation ENO1 cells than in the negative cells after 48h (t=8.54, P=0.01). The results indicate that ENO1 protein may be an important potential tumor-marker associated with the development of gastric cancer.

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Article: Efficacy and safety of bevacizumab for patients with advanced non-small cell lung cancer
by  Ping Xu, Hongmei Li, Xiaoyan Zhang
Cancer Cell Research 2017 4(14) 334-339; published online 27 April 2017
Abstract: To observe the efficacy and safety of bevacizumab in the treatment of advanced non-small cell lung cancer (NSCLC). We retrospectively analyzed 36 patients of Stage IV non-squamous non-small cell lung cancer from March 2015 to December 2016. All patients were treated with Bevacizumab combined with Pemetrexed ± Platinum. The efficacy and adverse reactions were observed and followed up. In 36 patients, 10 patients (27.8%) had partial response, 22 patients (61.1%) had stable disease and 4 (11.1%) had progressive disease. The objective response rate was 27.8% and the disease control rate was 88.9%. The median progression-free survival time was 7.3 months and the median overall survival time was 13.1 months. The most common bevacizumab-related adverse events were proteinuria, hemorrhage and hypertension. Most adverse events were relieved after symptomatic treatment, and severe adverse reactions (grade 3 or above) were rare. Bevacizumab has definite therapeutic effect for advanced NSCLC patients and most adverse reactions could be tolerated.

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Article: Chain length effect on penetration behavior of mPEG-PCL micelles using multicellular tumor spheroids
by  Chen Wei, Yan Liang, Tingting Zhang, Lutao Jiang, Yitong Li, Miao Yu, Jialing Dai, Jiao Liu, Yong Sun
Cancer Cell Research 2017 4(14) 340-345; published online 27 April 2017
Abstract: Four amphiphilic diblock copolymers with methoxy poly (ethylene glycol) (mPEG) and different chain lengths of polycaprolactone (PCL), encapsulated anticancer drug doxorubicin (DOX) on the hydropholic cores were fabricated. The 1H nuclear magnetic resonance(1H NMR), Gel Permeation Chromatography (GPC) were characterized to confirm the successful synthesis of the copolymeric micelles. In vitro cytotoxicity verify the micelles was non-toxic to cells and DOX loaded micelles shows efficient anticancer activity. The penetration behavior was might assist the diffusion of DOX, which was confirmed by confocal microscopy images. Results indicate that mPEG-PCL micelles were found to substantially provides an efficient antitumor carrier and reduce drawback of free DOX.

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Article: Autophagy alleviates LPS induced Hyper-Permeability of Caco-2 cells by regulating claudin-2 protein
by  Weiwei Wen, Hongbo Li, Luqiao Huang, Yingjian Jiang, Dehui Li, Yibo Liang, Dianliang Zhang
Cancer Cell Research 2017 4(14) 346-350; published online 27 April 2017
Abstract: To investigate the effect of autophagy on claudin-2 in lipopolysaccharide (LPS) induced hyper-permeability of intestinal epithelial cell. In human colon cancer cell line (Caco-2), the model of intestinal epithelial injury induced by LPS was established, which were LPS group, LPS combined with inhibitor of autophagy (3-Methyladenine, 3-MA) and control group. Transepithelial resistance (TER) was detected by Millicell-ERS and monolayer permeability was evaluated by paracellular transport of fluorescein isothiocyanate dextran (FITC-dextran).Expression of LC3II and claudins-2 in Caco-2 cells were analyzed by Western blot. Expression of mRNA of CL-2 was detected by RT-PCR. The results showed that LPSinduced the expression of LC3II was increased, and TER was decreased compared with control group. Moreover, claudin-2 and monolayer permeability were up-regulated in LPS + 3-MA group compared with LPS group, and TER was significantly decreased compared with LPS group and control group. Autophagy may down regulated the expression of CL-2 in intestinal epithelial cells induced by LPS, and reduce intestinal epithelial permeability to protect intestinal mucosal barrier.

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Article: HBx enhances cell viability, migration and invasion of hepatocellular carcinoma via PD-L1
by  Jinxin Tian, Junlei Liu, Jun Liang
Cancer Cell Research 2017 4(14) 351-355; published online 27 April 2017
Abstract: Programmed death 1 ligand (PD-L1) is expressed in many cancers. Many studies have confirmed that PD-L1 is involved in multiple behaviors of cancers, such as cell viability, proliferation, migration, invasion, apoptosis and immune escape. In hepatocellular carcinoma (HCC), some studies show that PD-L1 expression is related to HBx, which is encoded by the X gene in Hepatitis B virus (HBV). In our study, HBx gene was transfected into HepG2 cell (HBV negative cell line), expressing HBx protein. Moreover, the HBx gene was down-regulated through small interfering RNA (siRNA). Meanwhile, PD-L1 gene was also transfected into HepG2 cell alone. PD-L1-siRNA can decrease the expression of PD-L1. The results showed that the ability of cell viability, migration, and invasion was promoted when HBx and PD-L1 increased. However, the results were opposite when HBx and PD-L1 were inhibited. Confirmed results indicate that HBx enhances cell proliferation, migration and invasion of hepatocellular carcinoma via PD-L1. These studies suggest that knocking down HBx gene and blocking PD-1 (programmed death 1)/PD-L1 immune detection point may be expected as an immunotherapy for HBV positive HCC patients.

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Article: YAP mediate hypoxia-induced pancreatic cancer cells invasion and migration via promoting survivin expression
by  Xiaopeng Yang, Shanglong Liu Jianfei Xu, Shougen Cao, Yanbing Zhou
Cancer Cell Research 2017 4(14) 356-361; published online 27 April 2017
Abstract: Hypoxia microenvironment is considered to be a contributing factor to tumor invasion and metastasis. However, the molecular mechanism whereby hypoxia contributes to these events has not been completely elucidated. Here we showed that two pancreatic cancer (PC) cells, Panc-1 and SW1990, display different invasive and migratory abilities under hypoxia conditions (1%O2). We also showed that YAP activation was required as an important role to switch on hypoxia-induced epithelial-mesenchymal transition (EMT) and invasion of PC cells upon hypoxia. Additionly, we found that YAP activation induced survivin expression; specific inhibition of survivin could reduce EMT and suppress the invasion and migration of PC cells. In conclusion, hypoxia promotes PC cells (Panc-1 and SW1990) invasion and migration via YAP/survivin pathway, which may be a new therapeutic target of pancreatic cancer.

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