Li Dong¹, Tian Bo², Jin Xiaosheng³

Oncology Research, Vol.27, No.1, pp. 9-17, 2019, DOI:10.3727/096504018X15178732625479

Abstract THIS ARTICLE WAS WITHDRAWN BY THE PUBLISHERS IN OCTOBER 2020. More >

Wei-Zhen Liu, Nian Liu

Oncology Research, Vol.27, No.1, pp. 1-8, 2019, DOI:10.3727/096504018X15172738893959

Abstract Propofol has been widely used in lung cancer resections. Some studies have demonstrated that the effects of propofol might be mediated by microRNAs (miRNAs). This study aimed to investigate the effects and mechanisms of propofol on lung cancer cells by regulation of miR-1284. A549 cells were treated with different concentrations of propofol, while transfected with miR-1284 inhibitor, si-FOXM1, and their negative controls. Cell viability, migration, and invasion, and the expression of miR-1284, FOXM1, and epithelial–mesenchymal transition (EMT) factors were detected by CCK-8, Transwell, qRT-PCR, and Western blot assays, respectively. In addition, the regulatory and binding… More >

Juan Gu^*, Chang-fu Cui^†, Li Yang^‡, Ling Wang^*, Xue-hua Jiang^*

Oncology Research, Vol.27, No.2, pp. 193-202, 2019, DOI:10.3727/096504018X15150662230295

Abstract Colon cancer (CC) is the third most common cancer worldwide. Emodin is an anthraquinone-active substance that has the ability to affect tumor progression. Our study aims to explore the effects and the relevant mechanism of emodin on the invasion and migration of CC in vitro and in vivo. In our study, we found that emodin inhibited the invasion and migration abilities of RKO cells and decreased the expression of matrix metalloproteinase-7 (MMP-7), MMP-9, and vascular endothelial growth factor (VEGF) in a dose-dependent manner. Further research suggested that emodin inhibited EMT by increasing the mRNA level… More >

Ni Kou^*1, Sha Liu^*1, Xiaojie Li^*, Wuwei Li^*, Weijian Zhong^*, Lin Gui^*, Songling Chai^*, Xiang Ren^*, Risu Na^*, Tao Zeng^†, Huiying Liu^*

Oncology Research, Vol.27, No.2, pp. 173-182, 2019, DOI:10.3727/096504018X15202945197589

Abstract The long noncoding RNA (lncRNA) H19 has been described to participate in the metastasis of various tumors. Nevertheless, whether H19 promotes or impedes tongue squamous cell carcinoma (TSCC) cell migration and invasion remains controversial. Here we found that the expression of H19 was elevated in TSCC tissues compared with adjacent normal tissues. Moreover, we demonstrated that the expression of H19 was higher in metastasized tumors compared with unmetastasized tumors. Consistently, TSCC cells express higher levels of H19 than human squamous cells. Subsequently, depletion of H19 impaired the migration and invasion abilities of TSCC cells. Mechanistically, More >

Fan-Chun Meng, Jun-Kai Lin

Oncology Research, Vol.27, No.2, pp. 139-146, 2019, DOI:10.3727/096504018X15185747911701

Abstract Inhibition of tumor metastasis is one of the most important purposes in colorectal cancer (CRC) treatment. This study aimed to explore the effects of liquiritigenin, a flavonoid extracted from the roots of Glycyrrhiza uralensis Fisch, on HCT116 cell proliferation, invasion, and epithelial-to-mesenchymal transition (EMT). We found that liquiritigenin significantly inhibited HCT116 cell proliferation, invasion, and the EMT process, but had no influence on cell apoptosis. Moreover, liquiritigenin remarkably reduced the expression of runt-related transcription factor 2 (Runx2) in HCT116 cells. Overexpression of Runx2 obviously reversed the liquiritigenininduced invasion and EMT inhibition. Furthermore, liquiritigenin inactivated the More >

Hua Zhang^*, Xiuquan He^†, Wenfei Yu^†, Bingqing Yue^†, Ziting Yu^†, Ying Qin^*

Oncology Research, Vol.27, No.8, pp. 859-869, 2019, DOI:10.3727/096504017X15049209129277

Abstract As the noncatalytic subunit of mammalian DNA polymerase, mitotic arrest-deficient protein 2B (MAD2B) has been reported to play a role in cell cycle regulation, DNA damage tolerance, gene expression, and carcinogenesis. Although its expression is known to be associated with poor prognosis in several types of human cancers, the significance of MAD2B expression in lung malignancies is still unclear. Our study showed that MAD2B expression significantly increased in lung cancer, especially in the metastatic tissues. We also found that knockdown of MAD2B inhibited the migration, invasion, and epithelial–mesenchymal transition of lung cancer cells in vitro More >

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 More >

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.… More >

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… More >

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 More >