首页> 外文期刊>Oncology Research >Overexpression of miR-509 Increases Apoptosis and Inhibits Invasion via Suppression of Tumor Necrosis Factor-alpha in Triple-Negative Breast Cancer Hs578T Cells
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Overexpression of miR-509 Increases Apoptosis and Inhibits Invasion via Suppression of Tumor Necrosis Factor-alpha in Triple-Negative Breast Cancer Hs578T Cells

机译:miR-509的过表达通过抑制三阴性乳腺癌Hs578T细胞中的肿瘤坏死因子-α增加细胞凋亡并抑制侵袭。

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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 cell invasion of Hs578T cells. Moreover, tumor necrosis factor-alpha (TNF-alpha) was involved in miR-509-mediated suppressive effects of TNBC cells, as being treated with TNF-alpha could partially abolish the suppressive effects of miR-509. Collectively, these data suggest that miR-509 could reverse the malignant phenotype of TNBC cells, probably by suppressing TNF-alpha.
机译:三阴性乳腺癌(TNBC)与转移和死亡的高复发率相关。据报道,miR-509在许多癌症中均是肿瘤抑制因子,但尚未确认其在TNBC中的作用。在本文中,我们探讨了miR-509对TNBC细胞恶性表型的影响,包括增殖,凋亡,迁移和侵袭。我们用miR-509模拟物瞬时转染了TNBC细胞Hs578T。转染后,与乱序模拟转染的细胞相比,miR-509的表达上调了约50倍。miR-509的过表达抑制细胞增殖,诱导细胞凋亡并抑制Hs578T细胞的侵袭。此外,肿瘤坏死因子-α(TNF-α)参与了miR-509介导的TNBC细胞的抑制作用,因为用TNF-α治疗可以部分消除miR-509的抑制作用。总体而言,这些数据表明,miR-509可能通过抑制TNF-α来逆转TNBC细胞的恶性表型。

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