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  • Open Access

    ARTICLE

    Propofol Inhibits Lung Cancer A549 Cell Growth and Epithelial–Mesenchymal Transition Process by Upregulation of MicroRNA-1284

    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 relationships among propofol, miR-1284, and… More >

  • Open Access

    ARTICLE

    Emodin Inhibits Colon Cancer Cell Invasion and Migration by Suppressing Epithelial–Mesenchymal Transition via the Wnt/b-Catenin Pathway

    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 of E-cadherin and decreasing the… More >

  • Open Access

    ARTICLE

    H19 Facilitates Tongue Squamous Cell Carcinoma Migration and Invasion via Sponging miR-let-7

    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, we demonstrated that H19 functions… More >

  • Open Access

    ARTICLE

    Liquiritigenin Inhibits Colorectal Cancer Proliferation, Invasion, and Epithelial-to-Mesenchymal Transition by Decreasing Expression of Runt-Related Transcription Factor 2

    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 phosphoinositide 3-kinase/ protein kinase B… More >

  • Open Access

    ARTICLE

    NET1 Enhances Proliferation and Chemoresistance in Acute Lymphoblastic Leukemia Cells

    Hongbo Sun*1, Zhifu Zhang*1, Wei Luo*, Junmin Liu*, Ye Lou, Shengmei Xia

    Oncology Research, Vol.27, No.8, pp. 935-944, 2019, DOI:10.3727/096504019X15555388198071

    Abstract Acute lymphoblastic leukemia (ALL) is the most prevalent of pediatric cancers. Neuroepithelial cell-transforming 1 (NET1) has been associated with malignancy in a number of cancers, but the role of NET1 in ALL development is unclear. In the present study, we investigated the effect of NET1 gene in ALL cell proliferation and chemoresistance. We analyzed GEO microarray data comparing bone marrow expression profiles of pediatric B-cell ALL samples and those of age-matched controls. MTT and colony formation assays were performed to analyze cell proliferation. ELISA assays, Western blot analyses, and TUNEL staining were used to detect chemoresistance. We confirmed that NET1… More >

  • Open Access

    ARTICLE

    Mitotic Arrest-Deficient Protein 2B Overexpressed in Lung Cancer Promotes Proliferation, EMT, and Metastasis

    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 and the metastasis in vivo,… More >

  • Open Access

    ARTICLE

    PD-L1 Induces Epithelial–Mesenchymal Transition in Nasopharyngeal Carcinoma Cells Through Activation of the PI3K/AKT Pathway

    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

    miR-203 Inhibits the Invasion and EMT of Gastric Cancer Cells by Directly Targeting Annexin A4

    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

    OLFM4 Inhibits Epithelial–Mesenchymal Transition and Metastatic Potential of Cervical Cancer Cells

    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

    1,25(OH)2D3 Attenuates IL-1b-Induced Epithelial-to-Mesenchymal Transition Through Inhibiting the Expression of lncTCF7

    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 >

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