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  • 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.… 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 More >

  • Open Access

    ARTICLE

    Silencing of NADPH Oxidase 4 Attenuates Hypoxia Resistance in Neuroblastoma Cells SH-SY5Y by Inhibiting PI3K/Akt-Dependent Glycolysis

    Ting Yu*1, Lei Li†1, Wenyan Liu*, Bailiu Ya*, Hongju Cheng*, Qing Xin*

    Oncology Research, Vol.27, No.5, pp. 525-532, 2019, DOI:10.3727/096504018X15179668157803

    Abstract Hypoxia-induced chemoresistance is a major obstacle in the development of effective cancer therapy. In our study, the reversal abilities of NADPH oxidase 4 (NOX4) silence on hypoxia resistance and the potential mechanism were investigated. Our data showed that the expression of NOX4 was upregulated in human neuroblastoma cells SH-SY5Y under hypoxia condition time dependently. Knockdown of NOX4 expression by siRNA inhibited glycolysis induced by hypoxia through decreasing the expression of glycolysis-related proteins (HIF-1 , LDHA, and PDK1), decreasing glucose uptake, lactate production, and ROS production, while increasing mitochondria membrane potential. Moreover, NOX4 silence inhibited cell… More >

  • Open Access

    ARTICLE

    CD47 Promotes Human Glioblastoma Invasion Through Activation of the PI3K/Akt Pathway

    Xuejian Liu*1, Xia Wu*1, Yanming Wang, Yuhua Li*, Xiangli Chen*, Wenchuan Yang*, Lihua Jiang*

    Oncology Research, Vol.27, No.4, pp. 415-422, 2019, DOI:10.3727/096504018X15155538502359

    Abstract Cluster of differentiation 47 (CD47) overexpression is common in various malignancies. This study investigated whether CD47 promotes human glioblastoma invasion and, if so, the underlying mechanisms involved. CD47 expression was found to be stronger in tissues of patients with glioblastoma and in various cancer cell lines than in normal controls. CD47 downregulation via siRNA suppressed invasion in vitro, whereas CD47 overexpression through plasmid transfection exerted the opposite effect. However, overexpression or knocking down of CD47 had no effect on cell proliferation. Moreover, CD47 expression was related to Akt phosphorylation at the cellular molecular level. Suppression More >

  • Open Access

    ARTICLE

    Interaction of IL-22/IL-22R1 promotes cell proliferation and suppresses apoptosis of colorectal cancer via phosphorylation of STAT3

    Xiaoning Qin1, Liqing Yuan2, Hongxun Ruan1, Lin Lin1

    BIOCELL, Vol.43, No.2, pp. 89-98, 2019, DOI:10.32604/biocell.2019.06352

    Abstract Interleukin-22 (IL-22) is a member of IL-10 cytokine family which is expressed in activated T cells predominantly and in activated natural killer cells at lower levels. Previous studies have demonstrated the link between elevated levels of IL-22 and disease severity of psoriasis, Crohn’s disease, rheumatoid arthritis and interstitial lung diseases. However, the function of IL-22 in the development and progression of colorectal cancer (CRC) remains elusive. In this study, we first evaluated the IL-22/IL-22R1 level in CRC patients, and found that tumor tissues have more active expression of IL-22 and IL-22R1 than normal tissues,… More >

  • Open Access

    ARTICLE

    MicroRNA-204 Inhibits the Growth and Motility of Colorectal Cancer Cells by Downregulation of CXCL8

    Feng Shuai*, Bo Wang, Shuxiao Dong

    Oncology Research, Vol.26, No.8, pp. 1295-1305, 2018, DOI:10.3727/096504018X15172747209020

    Abstract Among all of the miRNAs, miR-204 has gained considerable attention in the field of cancer research. This study aimed to reveal the detailed functions and the underlying mechanism of miR-204 in colorectal cancer (CRC) cells. The expressions of miR-204 in CRC tumor tissues and cell lines were monitored. Expressions of miR-204 and CXCL8 in Caco-2 and HT-29 cells were altered by transfection, and then cell viability, apoptosis, migration, invasion, EMT-related protein expression, and PI3K/AKT/mTOR pathway protein expression were assessed. We found that miR-204 was expressed at low levels in CRC tumor tissues and cell lines… More >

  • Open Access

    ARTICLE

    Long Noncoding RNA FGFR3-AS1 Promotes Hepatocellular Carcinoma Carcinogenesis via Modulating the PI3K/AKT Pathway

    Juhua Zhuang*1, Saifei He*1, Guoyu Wang*, Guangdong Wang*†, Jing Ni*, Suiliang Zhang, Ying Ye*, Wei Xia*

    Oncology Research, Vol.26, No.8, pp. 1257-1265, 2018, DOI:10.3727/096504018X15172756878992

    Abstract Hepatocellular carcinoma (HCC) as one of the most refractory cancers leads to high mortality worldwide. Long noncoding RNAs have been widely acknowledged as important biomarkers and therapeutic targets in HCC. In this study, we investigated the effects of long noncoding RNA FGFR3-AS1 on tumor growth and metastasis in HCC. First, we found that the expression of FGFR3-AS1 was upregulated about threefold in HCC samples and cell lines. We knocked down FGFR3-AS1 in Huh7 and Hep3B cells and found that FGFR3-AS1 knockdown significantly inhibited cell proliferation but induced apoptosis. Moreover, FGFR3-AS1 knockdown led to more HCC More >

  • Open Access

    ARTICLE

    miR-135a Confers Resistance to Gefitinib in Non-Small Cell Lung Cancer Cells by Upregulation of RAC1

    Tingting Zhang*1, Ning Wang†1

    Oncology Research, Vol.26, No.8, pp. 1191-1200, 2018, DOI:10.3727/096504018X15166204902353

    Abstract The EGFR tyrosine kinase inhibitor gefitinib is used in therapy for non-small cell lung cancer (NSCLC). However, the therapeutic efficacy of gefitinib is known to be impeded by mutations of EGFR. The aim of the present study was to reveal the role of miR-135a in gefitinib resistance of NSCLC cells. Human NSCLC cell lines, NCI-H1650 and NCI-H1975, were transfected with miR-135a mimic/inhibitor or miR-135a inhibitor plus pEX-RAC1 (a RAC1-expressing vector). The effects of miR-135a and RAC1 expression on cell viability, apoptosis, migration, and invasion were then detected. The transfected cells were exposed to 0–20 µM… More >

  • Open Access

    ARTICLE

    Phosphoglycerate Mutase 1 (PGAM1) Promotes Pancreatic Ductal Adenocarcinoma (PDAC) Metastasis by Acting as a Novel Downstream Target of the PI3K/Akt/mTOR Pathway

    Xinlu Liu, Xiaodong Tan, Peng Liu, Yunhao Wu, Songying Qian, Xiaobo Zhang

    Oncology Research, Vol.26, No.7, pp. 1123-1131, 2018, DOI:10.3727/096504018X15166223632406

    Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive tumors known, with an overall 5-year survival rate of less than 6% due to early local invasion and distant metastasis. Exploring suitable therapeutic targets associated with invasion and metastasis is required for improving the prognosis of PDAC. In this study, we investigated the role of the glycolytic enzyme phosphoglycerate mutase 1 (PGAM1) in PDAC. PGAM1 expression was examined in tissue samples of 54 PDAC patients using immunohistochemistry, and the correlation between clinicopathological expression and PGAM1 expression was determined. A survival curve was generated using the… More >

  • Open Access

    ARTICLE

    Long Noncoding RNA ATB Promotes Proliferation, Migration, and Invasion in Bladder Cancer by Suppressing MicroRNA-126

    Xingquan Zhai, Wei Xu

    Oncology Research, Vol.26, No.7, pp. 1063-1072, 2018, DOI:10.3727/096504018X15152072098476

    Abstract This study aimed to explore the biological functions of long noncoding RNA activated by transforming growth factor-b (lncRNA-ATB) in bladder cancer cells. For the expressions of lncRNA-ATB, miR-126, and KRAS, T24 cells were transfected with their specific vectors/shRNA or mimic/inhibitor. Then cell viability, migration, invasion, and apoptosis as well as the protein levels of apoptosis-related factors and PI3K/AKT and mTOR signal pathways were measured. The relationships of lncRNA-ATB and miR-126 or miR-126 and KRAS were analyzed by Dual-Luciferase Reporter assay. Functional experiments showed that lncRNA-ATB overexpression significantly promoted cell viability, migration, and invasion in T24 More >

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