IL-17诱导的p300调控NSCLC细胞迁移、侵袭和MMP2生成的作用
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1.南京医科大学;2.南京医科大学第一附属医院

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IL-17-induced p300 regulates the migration, invasion and MMP2 production of NSCLC cells
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Nanjing Medical University

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    摘要:

    目的: 探讨IL-17刺激非小细胞肺癌(non-small cell lung cancer, NSCLC)细胞上调腺病毒E1A相关300 kDa蛋白(adenoviral E1A binding protein of 300 kDa, p300)调控其细胞迁移、侵袭及生成基质金属蛋白酶2(matrix metalloproteinase 2, MMP2)的作用。方法:用IL-17刺激 NSCLC细胞(H1299)后行划痕和Transwell实验观察细胞迁移和侵袭的变化。然后用western blot(WB)检查p300和MMP2蛋白的表达。同时,将p300过表达质粒(pcDNA3.1/p300)或shp300小干扰质粒转染H1299细胞(后者再行IL-17刺激),用前述方法测定细胞迁移、侵袭和MMP2的合成。结果:用IL-17刺激H1299细胞后能显著诱导其迁移和侵袭,并上调p300和MMP2的表达。过表达p300可增强细胞的迁移与侵袭,并提高MMP2的生成,但沉默p300基因后由IL-17诱导细胞的迁移和侵袭能力及MMP2的表达均显著降低。结论:IL-17上调的p300能促进H1299细胞的迁移与侵袭以及MMP2的生成。

    Abstract:

    Objective:To investigate the effects of adenovirus E1A associated 300 kDa protein (p300) to regulate cell migration, invasion and production of matrix metalloproteinase-2 (MMP2) on non-small cell lung cancer (NSCLC) cells upregulated by IL-17 stimulation. Methods: After NSCLC cells (H1299) incubated with IL-17, scratch and transwell experiments were performed to observe the cell migration and invasion. Then the p300 and MMP2 protein expression was detected using western blot (WB). Meantime, p300 overexpression plasmids (pcDNA3.1/p300) or short hairpin RNA (shp300) plasmids were transfected into H1299 cells (the latter was stimulated with IL-17), and the cell migration, invasion and MMP2 synthesis were again examined by the same method described above. Results:The levels of cell migration, invasion and p300 or MMP2 expression were obviously elevated in H1299 cells treated by IL-17. p300 overexpression could up-regulate the cell migration, invasion and MMP2 production, while p300 gene knockdown by shp300 in H1299 cells, the cell migration, invasion and MMP2 expression induced by IL-17 were significantly reduced. Conclusion:IL-17-upregulated p300 in H1299 cells can promote the cell migration, invasion and MMP2 production.

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  • 收稿日期:2021-06-28
  • 最后修改日期:2021-08-06
  • 录用日期:2022-02-25
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