Open Access
ARTICLE
Jian-Wei Wang, Xiao-Feng Wu, Xiao-Juan Gu, Xing-Hua Jiang
Oncology Research, Vol.27, No.9, pp. 979-986, 2019, DOI:10.3727/096504018X15336368805108
Abstract Cancer-associated fibroblasts (CAFs) play a predominant role in regulating tumor progression. Understanding
how CAFs communicate with osteosarcoma is crucial for developing novel approaches for osteosarcoma therapy. Exosomes are able to transmit messages between cells. In this study, we demonstrated that CAFs transfer
exosomes to osteosarcoma cells, which promotes osteosarcoma cell migration and invasion. Using a miRNA
microarray analysis, we identified 13 miRNAs that are significantly increased in exosomes derived from
cancer-associated fibroblasts (CAFs) and corresponding paracancer fibroblasts (PAFs). In vitro studies further validated that the levels of microRNA-1228 (miR-1228) were increased in CAFs, its secreted exosomes,
and in recipient osteosarcoma… More >
Open Access
ARTICLE
Meng Wang*1,
Xin Wang†1,
Yuan Li‡1,
Qiang Xiao§, Xiao-Hai Cui*, Guo-Dong Xiao*, Ji-Chang Wang¶,
Chong-Wen Xu#, Hong Ren*, Dapeng Liu*
Oncology Research, Vol.27, No.9, pp. 987-995, 2019, DOI:10.3727/096504018X15424918479652
Abstract The aim of this study was to investigate the potential biological activities of nutlin-3 in the regulation of growth
and proliferation of non-small cell lung cancer (NSCLC) stem cells (CSCs), which may help in sensitizing to
axitinib-induced apoptosis. Nutlin-3 induction of p53 expression was used to test its role in controlling the
cell division pattern and apoptosis of NSCLC cells. A549 cells and H460 cells were pretreated with nutlin-3
and then treated with either an Akt1 activator or shRNA-GSK3 , to investigate the potential role of p53 sensitization in the biological effects of axitinib. We also determined the expression levels… More >
Open Access
ARTICLE
Xue-Yi Yang, Ye Sheng
Oncology Research, Vol.27, No.9, pp. 997-1006, 2019, DOI:10.3727/096504018X15439207752093
Abstract Although miR-101 is involved in the development and progression of T-cell acute lymphoblastic leukemia
(T-ALL), the underlying molecular mechanisms remain unclear. In this article, we report that miR-101 expression was inversely correlated with CX chemokine receptor 7 (CXCR7) level in T-ALL. Introducing miR-101
inhibited T-ALL cell proliferation and invasion in vitro and suppressed tumor growth and lung metastasis in
vivo. CXCR7 was identified as a direct target of miR-101. The inhibitory effects of miR-101 were mimicked
and counteracted by CXCR7 depletion and overexpression, respectively. Mechanistically, miR-101 targets
CXCR7/STAT3 axis to reduce T-ALL growth and metastasis. Overall, these findings implied the… More >
Open Access
ARTICLE
Lihui Wang, Qi Li, Zhuo Ye, Baoping Qiao
Oncology Research, Vol.27, No.9, pp. 1007-1014, 2019, DOI:10.3727/096504018X15231148037228
Abstract Renal carcinoma greatly threatens human health, but the involved molecular mechanisms are far from complete
understanding. As a master oncogene driving the initiation of many other cancers, ZBTB7 has not been established to be associated with renal cancer. Our data revealed that ZBTB7 is highly expressed in renal carcinoma
specimens and cell lines, compared with normal cells. The silencing of ZBTB7 suppressed the proliferation
and invasion of renal cancer cells. ZBTB7 overexpression rendered normal cells with higher proliferation
rates and invasiveness. An animal study further confirmed the role of ZBTB7 in the growth of renal carcinoma. Moreover, miR-137 was identified… More >
Open Access
ARTICLE
Lili Zhao*, Yao Zhang*, Jiaoxia Liu*, Wei Yin†, Dan Jin‡, Dandan Wang*, Wei Zhang*
Oncology Research, Vol.27, No.9, pp. 1015-1023, 2019, DOI:10.3727/096504018X15247341491655
Abstract MicroRNAs (miRNAs) are short endogenous noncoding RNAs that frequently play vital roles in many cancer
types. Herein we demonstrated that miR-185 was remarkably downregulated in NSCLC tissues compared with
adjacent normal tissues. A lower level of miR-185 was associated with lymph node metastasis. Functional
assays showed that upregulation of miR-185 inhibited the proliferation, colony formation, and invasion capacities of NSCLC cells in vitro. Furthermore, we found that miR-185 suppressed the epithelial–mesenchymal
transition (EMT) process. Bioinformatics analysis and luciferase reporter gene assays revealed that Kruppellike factor 7 (KLF7) was the target of miR-185. Overexpression of miR-185 reduced the expression of KLF7… More >
Open Access
ARTICLE
Chao Jiang*, Xueyan Liu†, Meng Wang*, Guoyue Lv*, Guangyi Wang*
Oncology Research, Vol.27, No.9, pp. 1025-1034, 2019, DOI:10.3727/096504018X15456687424096
Abstract miR-802 has been reported to be dysregulated in multiple tumors and contribute to tumor progression. However,
its role in HCC was still largely unknown. The aim of this study is to investigate the function and mechanism
of miR-802 in HCC progression. The results showed that miR-802 was upregulated in the peripheral blood
and tumor tissue of HCC patients, and high levels of blood miR-802 predicted poor prognosis. miR-802 had
no effect on the proliferation and migration of HCC cell lines. Interestingly, the levels of CD8/CD28 and
regulated in development and DNA damage response 1 (REDD1) were declined along with the… More >
Open Access
ARTICLE
Zhiguo Wang*†1,
Zehui Fang‡1,
Runzhang Lu†, Hongli Zhao‡, Tiejun Gong†,
Dong Liu†, Luojia Hong‡, Jun Ma†, Mei Zhang*
Oncology Research, Vol.27, No.9, pp. 1035-1042, 2019, DOI:10.3727/096504019X15528367532612
Abstract Although arsenic trioxide (ATO) is a well-known antileukemic drug used for acute promyelocytic leukemia
treatment, the development of ATO resistance is still a big challenge. We previously reported that microRNA-
204 (miR-204) was involved in the regulation of acute myeloid leukemia (AML) cell apoptosis, but its role
in chemoresistance is poorly understood. In the present study, we showed that miR-204 was significantly
increased in AML cells after ATO treatment. Interestingly, the increased miR-204 level that was negatively correlated with ATO induced the decrease in cell viability and baculoviral inhibition of apoptosis protein repeatcontaining 6 (BIRC6) expression. Overexpression of miR-204 potentiated… More >
Open Access
ARTICLE
Qin Liu*†, Wei Wang†, Fangqiong Li†, Dongyang Yu‡, Chunfen Xu*, Hongbing Hu*
Oncology Research, Vol.27, No.9, pp. 1043-1050, 2019, DOI:10.3727/096504019X15560124931900
Abstract Triptolide, an extract of Tripterygium wilfordii, has been shown to have a potent anticancer activity. In the
present study, it was found that triptolide could effectively induce apoptosis and inhibit proliferation and invasion in malignant MDA-MB-231 breast cancer cells. The study focused on its effect on inhibiting invasion,
which has not been extensively reported to date. We predicted that triptolide may change invasion activity via
microRNAs (miRNAs), which have been recognized as important regulators of gene expression. miRNAome
variation in MDA-MB-231 cells with or without triptolide treatment demonstrated that miR-146a was upregulated following treatment with triptolide. Our previous studies have… More >
Open Access
ARTICLE
Haizhen Wang*, Zhenghua Tang*, Ting Li*, Menglu Liu*, Yong Li†, Baoling Xing*
Oncology Research, Vol.27, No.9, pp. 1051-1060, 2019, DOI:10.3727/096504019X15561873320465
Abstract Medroxyprogesterone (MPA) is used for the conservative treatment of endometrial cancer. Unfortunately, progesterone resistance seriously affects its therapeutic effect. The purpose of the current study was to investigate
the influence of deletion of AT-rich interactive domain 1A (ARID1A) in progesterone resistance in Ishikawa
cells. Ablation of ARID1A was conducted through the CRISPR/Cas9 technology. Acquired progesterone-resistant Ishikawa (Ishikawa-PR) cells were generated by chronic exposure of Ishikawa cells to MPA. The sensitivity
of the parental Ishikawa, Ishikawa-PR, and ARID1A-deficient cells to MPA and/or LY294002 was determined
using the Cell Counting Kit-8 (CCK-8) assay and flow cytometry analysis. In addition, Western blot analysis… More >
Open Access
ARTICLE
Ming Zhang, Baochang Shi, Kai Zhang
Oncology Research, Vol.27, No.9, pp. 1061-1068, 2019, DOI:10.3727/096504019X15565325878380
Abstract Deregulation of miR-186 and Twist1 has been identified to be involved in the progression of multiple cancers.
However, the detailed molecular mechanisms underlying miR-186-involved cholangiocarcinoma (CCA) are
still unknown. In this study, we found that miR-186 was downregulated in CCA tissues and cell lines, and
negatively correlated with the expression of Twist1 protein. In vitro assays demonstrated that miR-186 mimics repressed cell proliferation, in vivo tumor formation, and caused cell cycle arrest. miR-186 mimics also
inhibited the migration and invasion of CCLP1 and SG-231 cells. Mechanistically, the 3′-untranslated region
(3′-UTR) of Twist1 mRNA is a direct target of miR-186. Further,… More >
Open Access
ARTICLE
Zhongyuan Yin*, Lin Yang†, Feng Wu‡, Jinshuo Fan‡, Juanjuan Xu‡, Yang Jin‡, Guanghai Yang§
Oncology Research, Vol.27, No.9, pp. 1069-1077, 2019, DOI:10.3727/096504019X15566157027506
Abstract Cysteine oxidation occurs at the active site of deubiquitinases (DUBs) during many biologic signaling cascades. Here we report that hepatocellular carcinoma cells (HCCs) generated higher levels of endogenous
reactive oxygen species (ROS). This elevated ROS production was inhibited by NADPH oxidase inhibitor
diphenylene iodonium (DPI) and mitochondria electron chain inhibitor rotenone in HCC cells. Moreover, we
found that H2O2 could activate NF- B-dependent inflammatory effect through increased induction of matrix
metalloproteinase 2 (MMP2), MMP9, and intercellular adhesion molecule 1 (ICAM1) expression levels. In
addition, we found that H2O2 could prolong NF- B activation by suppressing the negative regulatory functions
of… More >
Open Access
ARTICLE
Kecheng Zhou*†1,
Jie Chen*†1,
Jiayu Wu*†1,
Yangxinzi Xu‡, Qiaoyun Wu*†, Jingjing Yue*†, Yu Song§,
Shengcun Li*†, Peng Zhou¶, Wenzhan Tu*†, Guanhu Yang*†, Songhe Jiang*†
Oncology Research, Vol.27, No.9, pp. 1079-1088, 2019, DOI:10.3727/096504019X15579146061957
Abstract Profilin 2 (PFN2) was found to be mainly expressed in neurons and involved in the development of the brain. In
recent years, emerging evidence indicated that PFN2 is also significantly upregulated in various cancers including head and neck cancer (HNSC) and influences cancer cell proliferation, migration, and invasion. However,
the role of PFN2 in HNSC development and progression remains unclear. The aim of our study was to investigate the role of PFN2 in the development of HNSC and its possible molecular mechanisms. Bioinformatics
showed that increased expression of PFN2 in tumors correlated highly with poor prognosis of HNSC patients.
Our… More >
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