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  • Open Access

    ARTICLE

    Knockdown of REV7 Inhibits Breast Cancer Cell Migration and Invasion

    Liu Feng*†, Wang Wei*, Zhang Heng, Han Yantao, Wang Chunbo

    Oncology Research, Vol.24, No.5, pp. 315-325, 2016, DOI:10.3727/096504016X14666990347590

    Abstract REV7 (also known as MAD2L2) is a multifunctional protein involved in DNA damage tolerance, cell cycle regulation, gene expression, and carcinogenesis. Although its expression is reportedly associated with poor prognosis in several kinds of human cancers, the significance of REV7 expression in breast malignancies is unclear. In this study, REV7 was found to be increased in breast cancer. We found that knockdown of REV7 inhibited the migration, invasion, and epithelial–mesenchymal transition (EMT) of breast cancer cells. Meanwhile, overexpression of REV7 promoted the migration, invasion, and EMT of breast cancer cells. As shown by Western blot, More >

  • Open Access

    ARTICLE

    Inhibition of ERK1/2 Signaling Impairs the Promoting Effects of TGF-β1 on Hepatocellular Carcinoma Cell Invasion and Epithelial–Mesenchymal Transition

    Ling Liu, Nianfeng Li, Qi Zhang, Jixiang Zhou, Ling Lin, Xinxin He

    Oncology Research, Vol.25, No.9, pp. 1607-1616, 2017, DOI:10.3727/096504017X14938093512742

    Abstract Transforming growth factor-b (TGF-β) and ERK signaling have been implicated in various human cancers including hepatocellular carcinoma, but the underlying mechanism remains largely unclear. In this study, we aimed to explore the role of ERK1/2 in the regulation of TGF-β’s promoting and suppressive activities in HCC cells. Our data showed that treatment with TGF-β1 enhanced invasion and epithelial–mesenchymal transition (EMT) in HCC HepG2 cells, accompanied with increased MMP9 production and activation of Smad2/3 and ERK1/2, but inhibited tumor cell proliferation. These effects were eliminated by treatment with SB431542, a TGF-β inhibitor. Afterward, treatment with the… More >

  • Open Access

    ARTICLE

    Silencing of Armadillo Repeat-Containing Protein 8 (ARMc8) Inhibits TGF-β-Induced EMT in Bladder Carcinoma UMUC3 Cells

    Xuan Liang*, Qun-Li Men, Yong-wei Li, He-Cheng Li§, Tie Chong§, Zhao-lun Li§

    Oncology Research, Vol.25, No.1, pp. 99-105, 2017, DOI:10.3727/096504016X14719078133609

    Abstract Armadillo repeat-containing protein 8 (ARMc8) is a key factor in regulating cell migration, proliferation, tissue maintenance, and tumorigenesis. However, its role in bladder cancer remains unknown. Thus, in this study we sought to investigate the effect of ARMc8 on the epithelial-to-mesenchymal transition (EMT) progress in bladder cancer cells induced by transforming growth factor-b1 (TGF-β1). Our results found that ARMc8 was highly expressed in bladder cancer cell lines. ARMc8 silencing inhibited the TGF-β1-induced migration and invasion and suppressed the EMT progress in bladder cancer cells. Furthermore, ARMc8 silencing inhibited the TGF-β1-induced expression of β-catenin, cyclin D1, More >

  • Open Access

    ARTICLE

    Radiosensitization of Non-Small Cell Lung Cancer Cells by Inhibition of TGF-β1 Signaling With SB431542 Is Dependent on p53 Status

    Yifan Zhao*†1, Longxiao Wang*1, Qianyi Huang*‡, Youqin Jiang*, Jingdong Wang*, Liyuan Zhang‡§, Ye Tian‡§, Hongying Yang

    Oncology Research, Vol.24, No.1, pp. 1-7, 2016, DOI:10.3727/096504016X14570992647087

    Abstract Although medically inoperable patients with stage I non-small cell lung cancer cells (NSCLC) are often treated with stereotactic body radiation therapy, its efficacy can be compromised due to poor radiosensitivity of cancer cells. Inhibition of transforming growth factor-β1 (TGF-β1) using LY364947 and LY2109761 has been demonstrated to radiosensitize cancer cells such as breast cancer, glioblastoma, and lung cancer. Our previous results have demonstrated that another potent and selective inhibitor of TGF-β1 receptor kinases, SB431542, could radiosensitize H460 cells both in vitro and in vivo. In the present study, we investigated whether SB431542 could radiosensitize other… More >

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