Home / Journals / OR / Vol.27, No.9, 2019
  • Open Access

    ARTICLE

    Exosomal miR-1228 From Cancer-Associated Fibroblasts Promotes Cell Migration and Invasion of Osteosarcoma by Directly Targeting SCAI

    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

    Nutlin-3-Induced Sensitization of Non-Small Cell Lung Cancer Stem Cells to Axitinib-Induced Apoptosis Through Repression of Akt1/Wnt Signaling

    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

    miR-101 Represses T-Cell Acute Lymphoblastic Leukemia by Targeting CXCR7/STAT3 Axis

    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

    ZBTB7/miR-137 Autoregulatory Circuit Promotes the Progression of Renal Carcinoma

    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

    miR-185 Inhibits the Proliferation and Invasion of Non-Small Cell Lung Cancer by Targeting KLF7

    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

    High Blood miR-802 Is Associated With Poor Prognosis in HCC Patients by Regulating DNA Damage Response 1 (REDD1)-Mediated Function of T Cells

    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

    MicroRNA-204 Potentiates the Sensitivity of Acute Myeloid Leukemia Cells to Arsenic Trioxide

    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

    Triptolide Inhibits Breast Cancer Cell Metastasis Through Inducing the Expression of miR-146a, a Negative Regulator of Rho GTPase

    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

    CRISPR/Cas9-Mediated Gene Knockout of ARID1A Promotes Primary Progesterone Resistance by Downregulating Progesterone Receptor B in Endometrial Cancer Cells

    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

    miR-186 Suppresses the Progression of Cholangiocarcinoma Cells Through Inhibition of Twist1

    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

    Reactive Oxygen Species-Mediated Cezanne Inactivation by Oxidation of its Catalytic Cysteine Residue in Hepatocellular Carcinoma

    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

    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 prognosis of HNSC patients. Our… More >

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