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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