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  • 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

    NOTCH3 Overexpression and Posttranscriptional Regulation by miR-150 Were Associated With EGFR–TKI Resistance in Lung Adenocarcinoma

    Youwei Zhang*, Bi Chen, Yongsheng Wang, Qi Zhao, Weijun Wu§, Peiying Zhang*, Liyun Miao, Sanyuan Sun*

    Oncology Research, Vol.27, No.7, pp. 751-761, 2019, DOI:10.3727/096504018X15372657298381

    Abstract Acquired resistance remains a key challenge in epidermal growth factor receptor (EGFR)–tyrosine kinase inhibitors (TKIs) therapy in lung adenocarcinoma (LUAD). Recent studies have shown that Notch signaling is associated with drug resistance. However, its role and possible mechanisms in EGFR-TKI resistance are not yet clear. In our study, we found that among four members of NOTCH1–4, only NOTCH3 was upregulated in LUAD tissues and TKI-resistant cell line (HCC827GR6). Knockdown of NOTCH3 by siRNA significantly inhibited proliferative ability, and decreased colony and sphere formation in HCC827GR6 cells. Then miR-150 was identified as a posttranscriptional regulator of… More >

  • Open Access

    ARTICLE

    Upregulated lncRNA CASC2 May Inhibit Malignant Melanoma Development Through Regulating miR-18a-5p/RUNX1

    Yankun Zhang*, Wei Qian*, Feng Feng, Qian Cao*, Yanqi Li*, Ying Hou*, Luyang Zhang*, Jufeng Fan*

    Oncology Research, Vol.27, No.3, pp. 371-377, 2019, DOI:10.3727/096504018X15178740729367

    Abstract This study aimed to investigate the effect and underlying mechanism of lncRNA CASC2 in malignant melanoma (MM). Expression of CASC2 in MM tissues and cells was detected. A375 cells were transfected with pc-CASC2, si-CASC2, miR-18a-5p inhibitor, or corresponding controls, and then cell proliferation, migration, and invasion were detected using MTT assay, colony formation assay, and Transwell analysis, respectively. The relationship of miR-18a-5p and CASC2 or RUNX1 was detected by luciferase reporter assay. The levels of CASC2 and RUNX1 were significantly reduced in MM tissues compared with normal skin tissues or cells, while the miR-18a-5p level… More >

  • Open Access

    ARTICLE

    miR-150 Suppresses Tumor Growth in Melanoma Through Downregulation of MYB

    Xiyan Sun*1, Chao Zhang†1, Yang Cao, Erbiao Liu*

    Oncology Research, Vol.27, No.3, pp. 317-323, 2019, DOI:10.3727/096504018X15228863026239

    Abstract miR-150 has been demonstrated to inhibit tumor progression in various human cancers, including colorectal cancer, ovarian cancer, and thyroid cancer. However, the role of miR-150 in melanoma remains to be determined. In this study, we found that miR-150 was underexpressed in melanoma tissues and cell lines. Through transfection of miR-150 mimics, we found that miR-150 significantly inhibited the proliferation, migration, and invasion of melanoma cells. In mechanism, we found that MYB was a target of miR-150 in melanoma cells. Overexpression of miR-150 significantly inhibited mRNA and protein levels of MYB in melanoma cells. Moreover, there More >

  • Open Access

    ARTICLE

    MicroRNA-1277 Inhibits Proliferation and Migration of Hepatocellular Carcinoma HepG2 Cells by Targeting and Suppressing BMP4 Expression and Reflects the Significant Indicative Role in Hepatocellular Carcinoma Pathology and Diagnosis After Magnetic Resonance Imaging Assessment

    Xinshan Cao*, Ling Xu, Quanyuan Liu*, Lijuan Yang, Na Li§, Xiaoxiao Li*

    Oncology Research, Vol.27, No.3, pp. 301-309, 2019, DOI:10.3727/096504018X15213058045841

    Abstract Our study aimed to investigate the roles and possible regulatory mechanism of miR-1277 in the development of hepatocellular carcinoma (HCC). HCC patients were identified from patients who were diagnosed with focal liver lesions using magnetic resonance imaging (MRI). The expression levels of miR-1277 in the serum of HCC patients and HepG2 cells were measured. Then miR-1277 mimic, miR-1277 inhibitor, or scramble RNA was transfected into HepG2 cells. The effects of miR-1277 overexpression and suppression on HepG2 cell proliferation, migration, and invasion were then investigated. Additionally, the expression levels of epithelial– mesenchymal transition (EMT)-related markers, including… 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. 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 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.… 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, 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… More >

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