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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

    Overexpression of miR-509 Increases Apoptosis and Inhibits Invasion via Suppression of Tumor Necrosis Factor-α in Triple-Negative Breast Cancer Hs578T Cells

    Guoqiang Zhang*1, Zengyan Liu†1, Yong Han*, Xiaohong Wang*, Zhenlin Yang*

    Oncology Research, Vol.24, No.4, pp. 233-238, 2016, DOI:10.3727/096504016X14648701447977

    Abstract Triple-negative breast cancer (TNBC) is associated with high recurrence rates of metastasis and death. miR-509 has been reported to be a tumor suppressor in many cancers, but its effect in TNBC has not yet been identified. In this article, we explored the effects of miR-509 on the malignant phenotype of TNBC cells, including proliferation, apoptosis, migration, and invasion. We transiently transfected TNBC cells, Hs578T, with miR-509 mimic. Upon transfection, the expression of miR-509 was upregulated about 50-fold compared with cells transfected with scramble mimic. Overexpression of miR-509 inhibited cell proliferation, induced cell apoptosis, and suppressed More >

  • Open Access

    ARTICLE

    Knockdown of microRNA-29a Changes the Expression of Heat Shock Proteins in Breast Carcinoma MCF-7 Cells

    Encieh Choghaei*, Gholamreza Khamisipour, Mojtaba Falahati*, Behrooz Naeimi, Majid Mossahebi-Mohammadi, Rahim Tahmasebi, Mojtaba Hasanpour, Shakib Shamsian, Zahra Sadat Hashemi§

    Oncology Research, Vol.23, No.1-2, pp. 69-78, 2015, DOI:10.3727/096504015X14478843952906

    Abstract Breast cancer is the most commonly occurring cancer among women. MicroRNAs as noncoding small RNA molecules play pivotal roles in cancer-related biological processes. Increased levels of microRNA-29a in the serum of breast cancer patients have been reported. Since heat shock proteins (HSPs) play important roles in cell events, the quantitative fluctuations in their cellular levels could be deemed as key indicators of how the exerted treatment alters cell behavior. In this regard, using an antisense small RNA, we attempted to investigate the effects of miR-29a knockdown on the expression of HSPs genes in the MCF-7… More >

  • Open Access

    ARTICLE

    miR-544a Promotes Breast Cancer Cell Migration and Invasion Reducing Cadherin 1 Expression

    Pengwei Lu, Yuanting Gu, Lin Li, Fang Wang, Xinguang Qiu

    Oncology Research, Vol.23, No.4, pp. 165-170, 2015, DOI:10.3727/096504016X14519157902726

    Abstract Accumulating evidence has reported the significant role of miRNAs in the underlying biology of tumors, including breast cancer. The purpose for this study was to investigate the potential effects of miR-544a in breast cancer migration and invasion. The human normal breast Hs578Bst cells and the human breast cancer MCF-7 and MDA-MB-231 cells were used to analyze the expression of miR-544a by RT-PCR. The effects of miR-544a on the two kinds of breast cancer cell migration and invasion were analyzed using the Matrigel and Transwell assay, respectively. miR-544a expression on the cell metastasis-related protein expression was More >

  • Open Access

    ARTICLE

    Neoadjuvant Chemotherapy in Triple Negative Breast Cancer: An Observational Study

    Zhiying Shao*†, Shalini Chaudhri, Meng Guo§, Longzhen Zhang, Daniel Rea#

    Oncology Research, Vol.23, No.6, pp. 291-302, 2015, DOI:10.3727/096504016X14562725373879

    Abstract Triple negative breast cancer (TNBC) is a phenotype of breast cancer with aggressive clinical behavior. Because of the absence of optimal treatment, the prognosis of this disease is poor. The main purpose of this study was to detect the response to neoadjuvant chemotherapy (NACT) in a TNBC cohort and compare the long-term survival between patients with and without pathological complete response (pCR). A total of 53 patients diagnosed with TNBC from 2005 to 2013 who received NACT at the University Hospital Birmingham were enrolled in this study. Overall survival (OS) and progression-free survival (PFS) were… More >

  • Open Access

    REVIEW

    Minireview: C2- and C4-position 17β-estradiol metabolites and their relation to breast cancer

    ANNIE JOUBERT1*, HERMIA VAN ZYL1, JOHANNES LAURENS2, MONA-LIZA LOTTERING1

    BIOCELL, Vol.33, No.3, pp. 137-140, 2009, DOI:10.32604/biocell.2009.33.137

    Abstract C2- and C4-position 17β-estradiol metabolites play an important role in breast carcinogenesis. 2-Hydroxyestradiol and 4-hydroxyestradiol are implicated in tumorigenesis via two pathways. These pathways entail increased cell proliferation and the formation of reactive oxygen species that trigger an increase in the likelihood of deoxyribonucleic acid mutations.
    2-Methoxyestradiol, a 17β-estradiol metabolite, however, causes induction of apoptosis in transformed and tumor cells; thus exhibiting an antiproliferative effect on tumor growth. The 4-hydroxyestradiol:2- methoxyestradiol and 2-hydroxyestradiol:2-methoxyestradiolratios therefore ought to be taken into account as possible indicators of carcinogenesis. More >

  • Open Access

    ARTICLE

    Inhibition of focal adhesion kinase by antisense oligonucleotides enhances the sensitivity of breast cancer cells to camptothecins

    T.H. Satoh2, T.A. Surmacz3, O. Nyormoi4, C.M. Whitacre1

    BIOCELL, Vol.27, No.1, pp. 47-55, 2003, DOI:10.32604/biocell.2003.27.047

    Abstract This study shows a strong association between cell attachment to substratum and activation of β1-integrin-signaling with resistance to the camptothecin derivative topotecan (TPT) in breast cancer cells. We propose a mechanistic-driven approach to sensitize the cells to camptothecins. ZR-75-1 anchoragedependent breast cancer cell line, its derivative 9D3S suspension cells (9D3S-S), and 9D3S cells attached to fibronectin-coated plates (9D3S-A) were treated with TPT (1 µM) or CPT-11 (40 µM) for 48 h. Programmed cell death (PCD), as shown by poly(ADP-ribose) polymerase (PARP), pro-caspase-3 and pro-caspase-9 cleavage, was observed in 9D3S-S cells but not in ZR-75-1 or More >

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