Home / Journals / OR / Vol.27, No.6, 2019
  • Open Access

    ARTICLE

    Kaempferol Suppresses Proliferation and Induces Cell Cycle Arrest, Apoptosis, and DNA Damage in Breast Cancer Cells

    Li Zhu*, Lijun Xue
    Oncology Research, Vol.27, No.6, pp. 629-634, 2019, DOI:10.3727/096504018X15228018559434
    Abstract Kaempferol is a flavonoid that has been extensively investigated owing to its antitumor effects. Nevertheless, little is known about its underlying mechanisms of action. We aimed to explore the role of kaempferol in breast cancer (BC), and thus we investigated how kaempferol suppresses the growth of BC cells. The cells were treated with kaempferol, and the effects on multiple cancer-associated pathways were evaluated. The MTS assay was used to study the cell growth inhibition induced by kaempferol. The cell cycle was analyzed by flow cytometry. Western blotting was used to analyze cellular apoptosis and DNA damage. We found that the… More >

  • Open Access

    ARTICLE

    Apatinib Plus Chemotherapy Shows Clinical Activity in Advanced NSCLC: A Retrospective Study

    Jing Tang*1, Xu Yong Li†1, Jing Bo Liang, De Wu§, Li Peng, Xiaobing Li
    Oncology Research, Vol.27, No.6, pp. 635-641, 2019, DOI:10.3727/096504018X15288447760357
    Abstract Apatinib is an oral TKI with antiangiogenic properties, and it is currently approved for the treatment of advanced gastric cancer in China. This agent has also been tested in other human solid tumors, including non-small cell lung cancer (NSCLC). Since the combination of chemotherapy and an antiangiogenic agent has been shown to be a feasible strategy in NSCLC, it is conceivable that a similar approach combining apatinib with chemotherapy may yield clinical activity. With this in mind, we investigated the efficiency of apatinib in combination with pemetrexed or docetaxel in advanced NSCLC. We treated a total of 20 patients with… More >

  • Open Access

    ARTICLE

    Heme Oxygenase-1 Inhibits Tumor Metastasis Mediated by Notch1 Pathway in Murine Mammary Carcinoma

    Qiang Li*†1, Qi Liu*1, Wanpeng Cheng*, Huiyan Wei*, Wenqian Jiang*, Fang E*, Yuan Yu*, Jianfeng Jin*, Chaoxia Zou*‡
    Oncology Research, Vol.27, No.6, pp. 643-651, 2019, DOI:10.3727/096504018X15415906335771
    Abstract Heme oxygenase-1 (HO-1) plays an important role in the progression of several malignancies including breast cancer. However, its role in breast cancer metastasis is still ambiguous. In this study, we observed the effect of HO-1 on mouse mammary carcinoma metastasis using the in vivo tumor metastasis model. Our results revealed that overexpression of HO-1 strongly inhibits the lung metastasis of 4T1 cells. In in vitro analysis, associated indices for epithelial–mesenchymal transition (EMT), migration, and proliferation of 4T1 cells were evaluated. The results show that HO-1 inhibits EMT, migration, and proliferation of 4T1 cells. In addition, the Notch1/ Slug pathway is… More >

  • Open Access

    ARTICLE

    Silencing of lncRNA AFAP1-AS1 Inhibits Cell Growth and Metastasis in Clear Cell Renal Cell Carcinoma

    Zhongyi Mu*†1, Dan Dong*1, Ning Wei‡§, Mingli Sun, Wei Wang*, Yue Shao*, Jian Gao*, Ping Yin*, Chenghai Zhao*
    Oncology Research, Vol.27, No.6, pp. 653-661, 2019, DOI:10.3727/096504018X15420748671075
    Abstract The lncRNA AFAP1-AS1, oriented from an antisense direction to the protein-coding gene AFAP1 in the opposite strand, was upregulated in a variety of tumors and associated with poor prognosis, including lung cancer, breast cancer, ovarian cancer, and so on. However, the biological role of AFAP1-AS1 in clear cell renal cell carcinoma (ccRCC) is still unknown. We observed that AFAP1-AS1 expression was significantly upregulated in ccRCC tissues and that patients with high-level expression of AFAP1-AS1 had a shorter overall survival. Knockdown of AFAP1-AS1 markedly suppressed the progression of proliferation, invasion, migration, and EMT in ccRCC cells. Downregulation of AFAP1-AS1 resulted in… More >

  • Open Access

    ARTICLE

    The Interaction Between lncRNA SNHG1 and miR-140 in Regulating Growth and Tumorigenesis via the TLR4/NF-kB Pathway in Cholangiocarcinoma

    Zhen Li*1, Xin Li*1, Xiao Du, Henghui Zhang, Zhengyang Wu*, Kewei Ren*, Xinwei Han*
    Oncology Research, Vol.27, No.6, pp. 663-672, 2019, DOI:10.3727/096504018X15420741307616
    Abstract Cholangiocarcinoma (CCA) is the second most common primary hepatobiliary carcinoma. The long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) has been reported to contribute to the progression of multiple cancers. Nonetheless, the functions and hidden mechanism of SNHG1 remain unclear in CCA. In this study, the SNHG1 levels were boosted in CCA cell lines, and knockdown of SNHG1 repressed CCA cell proliferation and invasion in vitro. The data also demonstrated that miR-140 could act as a target of SNHG1 in CCA and inhibited CCA cell proliferation and invasion, whereas the inhibition effects were relieved by overexpression of… More >

  • Open Access

    ARTICLE

    Knockdown of IARS2 Inhibited Proliferation of Acute Myeloid Leukemia Cells by Regulating p53/p21/PCNA/eIF4E Pathway

    Hong Li*1, Yaning Tian*1, Xiang Li*, Bin Wang, Dongzhi Zhai*, Yingying Bai*, Changhu Dong*, Xu Chao*‡
    Oncology Research, Vol.27, No.6, pp. 673-680, 2019, DOI:10.3727/096504018X15426261956343
    Abstract IARS2 encodes mitochondrial isoleucine-tRNA synthetase, which mutation may cause multiple diseases. However, the biological function of IARS2 on acute myeloid leukemia (AML) has not yet been identified. In the present study, qRT-PCR was used to determine the expression of IARS2 in K562, THP1, and HL-60 leukemia cells. Additionally the mRNA levels of IARS2 in CD34 cells and AML cells obtained from patients were detected by qRT-PCR. IARS2-shRNA lentiviral vector was established and used to infect acute myeloid leukemia HL-60 cells. qRT-PCR and Western blot analysis were employed to assess the knockdown effect of IARS2. The proliferation rate and cell cycle… More >

  • Open Access

    ARTICLE

    Knockdown of lncRNA PVT1 Inhibits Glioma Progression by Regulating miR-424 Expression

    Yanjie Han*1, Xinxin Li*1, Fei He†1, Jiliang Yan*, Chunyan Ma*, Xiaoli Zheng, Jinli Zhang*, Donghui Zhang*, Cuiping Meng*, Zhen Zhang*, Xinying Ji§
    Oncology Research, Vol.27, No.6, pp. 681-690, 2019, DOI:10.3727/096504018X15424939990246
    Abstract Plasmacytoma variability translocation 1 (PVT1), an oncogene, has been reported to be highly expressed in many tumors, including human glioma, gastric cancer, and non-small cell lung cancer. Functionally, it could also regulate the development of tumor cells. However, its specific roles and pathogenesis in human gliomas are still not clear. This study investigated the function and mechanism of PVT1 knockdown in the proliferation and malignant transformation of human gliomas. We first examined the expression levels of PVT1 and miR- 424 in human glioma tissues and cell lines. We also used gene manipulation techniques to explore the effects of PVT1 knockdown… More >

  • Open Access

    ARTICLE

    MicroRNA-101 Targets CXCL12-Mediated Akt and Snail Signaling Pathways to Inhibit Cellular Proliferation and Invasion in Papillary Thyroid Carcinoma

    Fang Chen*, Dongqiang Yang, Yuhua Ru, Shan Cao*, Aishe Gao*
    Oncology Research, Vol.27, No.6, pp. 691-701, 2019, DOI:10.3727/096504018X15426763753594
    Abstract Escalating evidence suggests that microRNA-101 (miR-101) is implicated in the development and progression of various cancers, including papillary thyroid carcinoma (PTC). However, the biological function and molecular mechanisms of miR-101 in PTC are still unclear. In this study, we demonstrated that miR-101 expression was significantly decreased in PTC tissues and cell lines. Clinically, a low level of miR-101 was positively associated with advanced histological stages and lymph node and distant metastases. The expression of CXCL12 was negatively correlated with miR-101 level in PTC. CXCL12 was validated as a direct target of miR-101 in PTC cells. Functional experiments proved that miR-101… More >

  • Open Access

    ARTICLE

    miR-374a Inhibitor Enhances Etoposide-Induced Cytotoxicity Against Glioma Cells Through Upregulation of FOXO1

    Wei Ni*†‡, Lin Luo*†‡, Ping Zuo*†‡, Renping Li*†‡, Xiaobing Xu*†‡, Fan Wen*†‡, Dong Hu*†‡
    Oncology Research, Vol.27, No.6, pp. 703-712, 2019, DOI:10.3727/096504018X15426775024905
    Abstract Glioma is a commonly diagnosed brain tumor that shows high mortality rate. Despite the great advancement of cancer therapy in recent years, chemotherapy is still an important approach for treatment of glioma. However, long-term chemotherapy usually causes serious side effects or complications. It is desirable to take strategies to enhance the efficacy of current chemotherapy. In the present study, we observed obvious upregulation of miR-374a in glioma cells. More importantly, we found that knockdown of miR-374a was able to enhance the etoposide-induced cytotoxicity against glioma cells. Mechanically, we demonstrated that FOXO1 was the target of miR-374a in glioma. Treatment with… More >

  • Open Access

    ARTICLE

    Extracellular S100A11 Plays a Critical Role in Spread of the Fibroblast Population in Pancreatic Cancers

    Hitoshi Takamatsu*1, Ken-ichi Yamamoto*1, Nahoko Tomonobu*, Hitoshi Murata*, Yusuke Inoue, Akira Yamauchi, I Wayan Sumardika, Youyi Chen*, Rie Kinoshita*, Masahiro Yamamura, Hideyo Fujiwara#, Yosuke Mitsui*, **, Kota Araki*††, Junichiro Futami‡‡, Ken Saito§§, Hidekazu Iioka§§, I Made Winarsa Ruma§, Endy Widya Putranto¶¶, Masahiro Nishibori##, Eisaku Kondo§§, Yasuhiko Yamamoto***, Shinichi Toyooka††, Masakiyo Sakaguchi*
    Oncology Research, Vol.27, No.6, pp. 713-727, 2019, DOI:10.3727/096504018X15433161908259
    Abstract The fertile stroma in pancreatic ductal adenocarcinomas (PDACs) has been suspected to greatly contribute to PDAC progression. Since the main cell constituents of the stroma are fibroblasts, there is crosstalking(s) between PDAC cells and surrounding fibroblasts in the stroma, which induces a fibroblast proliferation burst. We have reported that several malignant cancer cells including PDAC cells secrete a pronounced level of S100A11, which in turn stimulates proliferation of cancer cells via the receptor for advanced glycation end products (RAGE) in an autocrine manner. Owing to the RAGE+ expression in fibroblasts, the extracellular abundant S100A11 will affect adjacent fibroblasts. In this… 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/ -catenin signaling by promoting the… More >

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