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Search Results (8)
  • Open Access

    ARTICLE

    Knockdown of Long Noncoding RNA CAT104 Inhibits the Proliferation, Migration, and Invasion of Human Osteosarcoma Cells by Regulating MicroRNA-381

    Bo Xia*, Lei Wang, Li Feng*, Baofang Tian*, Yuanjie Tan, Baoyin Du*

    Oncology Research, Vol.27, No.1, pp. 89-98, 2019, DOI:10.3727/096504018X15199511344806

    Abstract Osteosarcoma is the most common primary malignant bone tumor in children and adolescents. This study aimed to explore the effects of long noncoding RNA CAT104 and microRNA-381 (miR-381) on osteosarcoma cell proliferation, migration, invasion, and apoptosis, as well as the underlying potential mechanism. We found that CAT104 was highly expressed in osteosarcoma MG63 and OS-732 cells. Knockdown of CAT104 significantly inhibited OS-732 cell proliferation, migration, and invasion, but promoted cell apoptosis. CAT104 regulated the expression of miR-381, and miR-381 participated in the effects of CAT104 on OS-732 cells. Zinc finger E-box-binding homeobox 1 (ZEB1) was More >

  • Open Access

    ARTICLE

    Emodin Inhibits Colon Cancer Cell Invasion and Migration by Suppressing Epithelial–Mesenchymal Transition via the Wnt/β-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… More >

  • Open Access

    ARTICLE

    Profilin 2 Promotes Proliferation and Metastasis of Head and Neck Cancer Cells by Regulating PI3K/AKT/b-Catenin Signaling Pathway

    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… More >

  • Open Access

    ARTICLE

    Inhibition of Proliferation by Knockdown of Transmembrane (TMEM) 168 in Glioblastoma Cells via Suppression of Wnt/β-Catenin Pathway

    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… More >

  • Open Access

    ARTICLE

    Synergistic Efficacy of the Demethylation Agent Decitabine in Combination With the Protease Inhibitor Bortezomib for Treating Multiple Myeloma Through the Wnt/b-Catenin Pathway

    Yulong Jin*, Li Xu*, Xiaodong Wu, Juan Feng*, Mimi Shu*, Hongtao Gu*, Guangxun Gao*, Jinyi Zhang, Baoxia Dong*, Xiequn Chen*

    Oncology Research, Vol.27, No.6, pp. 729-737, 2019, DOI:10.3727/096504018X15443011011637

    Abstract Multiple myeloma (MM) is a hematopoietic malignancy characterized by the clonal proliferation of antibodysecreting plasma cells. Bortezomib (BZM), the first FDA-approved proteasome inhibitor, has significant antimyeloma activity and prolongs the median survival of MM patients. However, MM remains incurable predominantly due to acquired drug resistance and disease relapse. -Catenin, a key effector protein in the canonical Wnt signaling pathway, has been implicated in regulating myeloma cell sensitivity to BZM. Decitabine (DAC) is an epigenetic modulating agent that induces tumor suppressor gene reexpression based on its gene-specific DNA hypomethylation. DAC has been implicated in modulating Wnt/… More >

  • Open Access

    ARTICLE

    Astragaloside IV Inhibits the Progression of Non-Small Cell Lung Cancer Through the Akt/GSK-3β/β-Catenin Pathway

    Liwei Jia*, Dongying Lv, Shuang Zhang*, Zhenyue Wang*, Bo Zhou*

    Oncology Research, Vol.27, No.4, pp. 503-508, 2019, DOI:10.3727/096504018X15344989701565

    Abstract Astragaloside IV (AS-IV) is an active ingredient in Astragalus membranaceus and is involved in various biological processes, such as regulating the immune system, and counteracting inflammation and malignancy. The aim of this study was to explore the effect of AS-IV on non-small cell lung cancer (NSCLC) cells. Cell counting kit (CCK)-8 assay and flow cytometry were performed to investigate cell survival and cell death, and Western blotting was performed to assess protein expression. We found that AS-IV inhibited the migration and proliferation of NSCLC cells and caused a noticeable increase in cell death. Furthermore, the More >

  • Open Access

    ARTICLE

    Ectopic Expression of miR-147 Inhibits Stem Cell Marker and Epithelial–Mesenchymal Transition (EMT)-Related Protein Expression in Colon Cancer Cells

    Xiaofei Ning*, Cong Wang, Meng Zhang, Kecheng Wang*

    Oncology Research, Vol.27, No.4, pp. 399-406, 2019, DOI:10.3727/096504018X15179675206495

    Abstract Colon cancer is one of the most common cancers in the world. Epithelial-to-mesenchymal transition (EMT) is a crucial step in tumor progression and is also involved in the acquisition of stem cell-like properties. Some miRNAs have been shown to function as either tumor suppressors or oncogenes in colon cancer. Here we investigated the role of miR-147 in the regulation of the stem cell-like traits of colon cancer cells. We observed that miR-147 was downregulated in several colon cancer cell lines, and overexpressed miR-147 decreased the expression of cancer stem cell (CSC) markers OCT4, SOX2, and… More >

  • Open Access

    ARTICLE

    Knockdown of Upregulated Gene 11 (URG11) Inhibits Proliferation, Invasion, and b-Catenin Expression in Non-Small Cell Lung Cancer Cells

    Zhe-liang Liu*, Jiao Wu, Lin-xian Wang, Jin-feng Yang, Gao-ming Xiao*, Hui-ping Sun, Yue-jun Chen*

    Oncology Research, Vol.24, No.3, pp. 197-204, 2016, DOI:10.3727/096504016X14648701447850

    Abstract Upregulated gene 11 (URG11), a new gene upregulated by hepatitis B virus X protein, was found to be involved in the development and progression of several tumors. However, the role of URG11 in human non-small cell lung cancer (NSCLC) has not yet been determined. Therefore, the aim of the present study was to explore the role of URG11 in human NSCLC. Our results found that URG11 was highly expressed in human NSCLC tissues compared with matched normal lung tissues, and higher levels were found in NSCLC cell lines in comparison to the normal lung cell More >

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