Open Access
ARTICLE
Tengyu Li, Jing Zhu, Shuai Zuo, Shanwen Chen, Ju Ma, Yongchen Ma, Shihao Guo,
Pengyuan Wang, Yucun Liu
Oncology Research, Vol.27, No.7, pp. 739-750, 2019, DOI:10.3727/096504018X15360541345000
Abstract The activated form of vitamin D3, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], regulates numerous cellular
processes, including inhibition of cancer progression. IL-1 has been reported to facilitate cancer development, especially by inducing an epithelial-to-mesenchymal transition (EMT) in several malignant tumors.
However, the underlying mechanism of 1,25(OH)2D3 and IL-1 in colorectal cancer (CRC) still remains
largely unknown. To fill in this knowledge gap, we measured cell proliferation and invasion by CCK-8 and
Transwell assays after stimulation with 1,25(OH)2D3 and IL-1 . E-cadherin and vimentin were chosen as
markers of EMT measured by immunofluorescence, quantitative real-time PCR (qRT-PCR), and Western
blot. The expression and function… More >
Open Access
ARTICLE
Youwei Zhang*, Bi Chen†, Yongsheng Wang‡, Qi Zhao‡, Weijun Wu§, Peiying Zhang*,
Liyun Miao‡, Sanyuan Sun*
Oncology Research, Vol.27, No.7, pp. 751-761, 2019, DOI:10.3727/096504018X15372657298381
Abstract Acquired resistance remains a key challenge in epidermal growth factor receptor (EGFR)–tyrosine kinase
inhibitors (TKIs) therapy in lung adenocarcinoma (LUAD). Recent studies have shown that Notch signaling
is associated with drug resistance. However, its role and possible mechanisms in EGFR-TKI resistance are
not yet clear. In our study, we found that among four members of NOTCH1–4, only NOTCH3 was upregulated in LUAD tissues and TKI-resistant cell line (HCC827GR6). Knockdown of NOTCH3 by siRNA significantly inhibited proliferative ability, and decreased colony and sphere formation in HCC827GR6 cells. Then
miR-150 was identified as a posttranscriptional regulator of NOTCH3. Its expression was downregulated… More >
Open Access
ARTICLE
Juan Li*†1,
Chunyan Liu‡1,
Dawei Li§, Meng Wan¶, Hong Zhang†, Xiaoxia Zheng†, Xuemei Jie†,
Pengju Zhang¶, Jingjing Li#, Hongchun Hou†, Qing Sun*
Oncology Research, Vol.27, No.7, pp. 763-771, 2019, DOI:10.3727/096504018X15399955297355
Abstract OLFM4 has been shown to play an important role in tumor initiation and progression. This study aims to
investigate the role of OLFM4 in metastatic cervical cancer and its underlying mechanism. Here we discover
that OLFM4 expression is significantly reduced in metastatic cervical cancer. Accordingly, overexpression of
OLFM4 inhibits epithelial–mesenchymal transition (EMT), migration, and invasion in human cervical cancer
cells. To further explore its molecular mechanisms, we reveal that OLFM4 augmentation interferes with mTOR
signaling pathway, and the suppressive effects of OLFM4 on cell migration and invasion are largely weakened
by phosphatidic acid (PA)-induced mTOR signal activation, which implicates the… More >
Open Access
ARTICLE
Teng Liu*, Juan Xu†, Hong Li Yan‡, Feng Chun Cheng*, Xi Jie Liu*
Oncology Research, Vol.27, No.7, pp. 773-778, 2019, DOI:10.3727/096504018X15208986577685
Abstract Luteolin, which is found in plant foods, has a range of therapeutic applications. In order to examine the potential roles of luteolin in ovarian teratocarcinoma, the human ovarian teratocarcinoma cell line PA-1 was selected
for functional experiments in vitro and in vivo. We demonstrated that luteolin inhibited the proliferation and
colony formation of PA-1 cells in vitro. The flow cytometry results suggested that luteolin induced apoptosis
of PA-1 cells in a dose-dependent manner. Immunofluorescence and qRT-PCR results showed that the expression of B-cell lymphoma-2 (Bcl-2) was decreased in luteolin-treated cells, whereas the expression of Bcl-2-
associated X (Bax) was increased… More >
Open Access
ARTICLE
Qiuying Quan*1,
Fengyun Zhong†1,
Xinwei Wang‡, Kai Chen§, Lingchuan Guo*
Oncology Research, Vol.27, No.7, pp. 779-788, 2019, DOI:10.3727/096504018X15442985680348
Abstract The aim of this study was to investigate the underlying mechanisms that transforming growth factor-
(TGF- )-mediated epithelial-to-mesenchymal transition (EMT) in tumor cells contributes to 5-FU resistance.
A series of experiments involving cell viability and caspase activity analyses, siRNA transfection, RNA isolation, and quantitative-PCR (qPCR) assay, cell migration analysis, Western blotting analysis of total protein and
membrane protein were performed in this study. Mouse xenograft model was used to determine the effect of
the PAR2 inhibitor in vivo. In this study, we found that protease-activated receptor 2 (PAR2) induction in 5-FU
therapy is correlated with TGF- -mediated EMT and apoptosis… More >
Open Access
ARTICLE
Jianye Li*, Bin Zhang†, Jizhao Cui‡, Zhen Liang§, Kexia Liu*
Oncology Research, Vol.27, No.7, pp. 789-799, 2019, DOI:10.3727/096504018X15444387696532
Abstract Many studies have shown that downregulated miR-203 level is in a variety of cancers including gastric cancer
(GC). However, the precise molecule mechanisms of miR-203 in GC have not been well clarified. In the current study, we investigated the biological functions and molecular mechanisms of miR-203 in GC cell lines.
We found that miR-203 is downregulated in GC tissues and cell lines. Moreover, the low level of miR-203
was associated with increased expression of annexin A4 in GC tissues and cell lines. The invasion and EMT
of GC cells were suppressed by overexpression of miR-203. However, downregulation of miR-203 promoted… More >
Open Access
ARTICLE
Zhenghua Fei*1,
Zhenxiang Deng†1,
Lingyang Zhou‡, Kejie Li*, Xiaofang Xia*, Raoying Xie*
Oncology Research, Vol.27, No.7, pp. 801-807, 2019, DOI:10.3727/096504018X15446984186056
Abstract Nasopharyngeal cancer (NPC) is a malignant epithelial carcinoma of the head and neck. Cancer therapy
targeting programmed cell death protein-1 (PD-1) or programmed death ligand-1 (PD-L1) is revolutionary.
However, the tumorigenic mechanism of PD-L1 is not yet clear in NPC. Here we demonstrated an oncogenic
role of PD-L1 via activating PI3K/AKT in NPC cells. PD-L1 overexpression was frequently detected in NPC
biopsies and cell lines by qRT-PCR. PD-L1 overexpression and knockdown demonstrated that PD-L1 promoted NPC cell invasion and metastasis in vitro and in vivo. Mechanistically, PD-L1 prominently activated the
epithelial–mesenchymal transition (EMT) process in a PI3K/AKT-dependent manner. Taken together,… More >
Open Access
ARTICLE
Juanjuan Yao*, Liang Zhong†, Pengqiang Zhong*, Dongdong Liu†, Zhen Yuan†, Junmei Liu*,
Shifei Yao*, Yi Zhao*, Min Chen*, Lianwen Li*, Lu Liu†, Beizhong Liu*†
Oncology Research, Vol.27, No.7, pp. 809-818, 2019, DOI:10.3727/096504018X15451301487729
Abstract RAS-responsive element-binding protein 1 (RREB1) is a transcription factor that is implicated in RAS
signaling and multiple tumors. However, the role of RREB1 in acute myeloid leukemia has not been studied.
We found that RREB1 is overexpressed in AML patients and myeloid leukemia cell lines (NB4 and HL-60),
and RREB1 expression was significantly decreased during granulocytic differentiation of myeloid leukemia
cells induced by all-trans retinoic acid (ATRA). Then we performed a RREB1 knockdown assay in NB4 and
HL-60 cells; the results showed that knockdown of RREB1 upregulated expression of CD11b, CEBP , and
microRNA-145 (miR-145), which hinted that knockdown of… More >
Open Access
ARTICLE
Jie Xu*1,
Zhongzhou Su*1,
Qiuping Ding†, Liang Shen*, Xiaohu Nie*, Xuyan Pan*, Ai Yan*,
Renfu Yan*, Yue Zhou*, Liqin Li‡, Bin Lu*
Oncology Research, Vol.27, No.7, pp. 819-826, 2019, DOI:10.3727/096504018X15478559215014
Abstract Human glioblastoma multiforme (GBM) accounts for the majority of human brain gliomas. Several TMEM
proteins, such as TMEM 45A, TMEM 97, and TMEM 140, are implicated in human brain gliomas. However,
the roles of TMEM168 in human GBM remain poorly understood. Herein we found that mRNA levels of
TMEM168 were overexpressed in GBM patients (n=85) when compared with healthy people (n=10),
which was also supported by data from The Cancer Genome Atlas (TCGA). Kaplan–Meier analysis of Gene
Expression Omnibus dataset GSE16011 suggested that enhanced TMEM168 expression was associated with
shorter survival time. To investigate whether and how TMEM168 functioned in… More >
Open Access
ARTICLE
Qing Wei1,
Rui Zhu1,
Junying Zhu, Rongping Zhao, Min Li
Oncology Research, Vol.27, No.7, pp. 827-834, 2019, DOI:10.3727/096504018X15462920753012
Abstract Emerging evidence suggests that 17β-estradiol (E2) and estrogen receptor (ER) signaling are protective against
hepatocellular carcinoma (HCC). In our previous study, we showed that E2 suppressed the carcinogenesis and
progression of HCC by targeting NLRP3 inflammasome activation, whereas the molecular mechanism by which
the NLRP3 inflammasome initiated cancer cell death was not elucidated. The present study aimed to investigate
the effect of NLRP3 inflammasome activation on cell death pathways and autophagy of HCC cells. First, we
observed an increasing mortality in E2-treated HCC cells, and then apoptotic and pyroptotic cell death were
both detected. The mortality of HCC cells was… More >
Open Access
ARTICLE
Hyun-Jung Moon,1
So-Young Park,1
Su-Hoon Lee, Chi-Dug Kang, Sun-Hee Kim
Oncology Research, Vol.27, No.7, pp. 835-847, 2019, DOI:10.3727/096504019X15517850319579
Abstract Recently, novel therapeutic strategies have been designed with the aim of killing cancer stem-like cells (CSCs),
and considerable interest has been generated in the development of specific therapies that target stemnessrelated marker of CSCs. In this study, nonsteroidal anti-inflammatory drugs (NSAIDs) significantly potentiated Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG)-mediated cytotoxicity through
apoptotic and autophagic cell death induction, but COX-2-inhibitory function was not required for NSAIDinduced autophagy in CD44-overexpressing human chronic myeloid leukemia K562 (CD44highK562) cells.
Importantly, we found that treatment with NSAIDs resulted in a dose-dependent increase in LC3-II level and
decrease in p62 level and simultaneous reduction in multiple stemness-related markers… More >
Open Access
REVIEW
Jie Wei*†1,
Yuanliang Yan*†1,
Xi Chen*†, Long Qian*†, Shuangshuang Zeng*†, Zhi Li‡,
Shuang Dai*†, Zhicheng Gong*†,Zhijie Xu§
Oncology Research, Vol.27, No.7, pp. 849-858, 2019, DOI:10.3727/096504018X15447833065047
Abstract Over the past decade, natural compounds have been proven to be effective against many human diseases,
including cancers. Triptolide (TPL), a diterpenoid triepoxide from the Chinese herb Tripterygium wilfordii
Hook F, has exhibited attractive cytotoxic activity on several cancer cells. An increasing number of studies have emphasized the antitumor effects of TPL on non-small cell lung cancer (NSCLC). Here we mainly
focused on the key molecular signaling pathways that lead to the inhibitory effects of TPL on human NSCLC,
such as mitogen-activated protein kinases (MAPKs) modulation, inhibition of NF- B activation, suppression
of miRNA expression, etc. In addition, the effect… More >
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