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  • 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 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

    miR-365 Suppresses Cholangiocarcinoma Cell Proliferation and Induces Apoptosis by Targeting E2F2

    Lunjian Chen*, Xiaorong Huang, Xinxin Chen

    Oncology Research, Vol.26, No.9, pp. 1375-1382, 2018, DOI:10.3727/096504018X15188352857437

    Abstract Cholangiocarcinoma (CCA) is one of the most malignant adenocarcinomas arising from bile duct epithelial cells. However, the molecular mechanism regulating CCA development and progression still needs to be investigated. Here we found that miR-365 was downregulated in CCA tissues compared with adjacent normal tissues. By functional experiments, we found that overexpression of miR-365 significantly inhibited CCA cell proliferation and promoted cellular apoptosis in vitro. Furthermore, administration with miR-365 markedly suppressed the growth of tumor tissues in vivo. Mechanistically, we identified E2F2 as the target gene of miR- 365 in CCA cells. We found that overexpression More >

  • Open Access

    ARTICLE

    Long Noncoding RNA NEAT1 Promotes Growth and Metastasis of Cholangiocarcinoma Cells

    Cheng Zhang*, Jing-Yi Li*, Fu-Zhou Tian, Gang Zhao, Hai Hu, Yue-Feng Ma*, Yu-Long Yang*

    Oncology Research, Vol.26, No.6, pp. 879-888, 2018, DOI:10.3727/096504017X15024935181289

    Abstract Long noncoding RNAs (lncRNAs) are known to play important roles in cancers. However, little is known about lncRNAs in cholangiocarcinoma (CCA), a cholangiocyte malignancy with poor prognosis. We investigated the role of nuclear paraspeckle assembly transcript 1 (NEAT1) lncRNA in promoting CCA. qRT-PCR analysis of patient samples showed that NEAT1 expression was higher in CCA tumors than in matched adjacent nontumor tissue. NEAT1 levels were also higher in CCA cell lines than in a normal biliary epithelium cell line (HIBEpic). NEAT1 knockdown in CCA cell lines using shNEAT1 reduced cell proliferation and colony formation in… More >

  • Open Access

    ARTICLE

    Inhibition of NF-kB Activity Enhances Sensitivity to Anticancer Drugs in Cholangiocarcinoma Cells

    Wunchana Seubwai*†‡, Kulthida Vaeteewoottacharn‡§, Ratthaphol Kraiklang, Kazuo Umezawa#, Seiji Okada**, Sopit Wongkham‡§

    Oncology Research, Vol.23, No.1-2, pp. 21-28, 2015, DOI:10.3727/096504015X14424348426071

    Abstract Cholangiocarcinoma (CCA) is a dismal cancer. At present, there is no effective chemotherapeutic regimen for CCA. This may be due to the marked resistance of CCA to chemotherapy drugs, for which a mechanism remains unknown. Nuclear factor-kB (NF-kB) is constitutively activated in a variety of cancer cells, including CCA. It has been shown to play roles in growth, metastasis, and chemoresistance of cancer. In the present study, we examined whether NF-kB is involved in the chemoresistance of CCA and whether dehydroxymethylepoxyquinomicin (DHMEQ), an effective NF-kB inhibitor, can overcome the drug resistance of CCA. Two CCA… More >

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