MiR-9 is involved in TGF-β1-induced lung cancer cell invasion and adhesion by targeting SOX7.
MiR-9 is involved in TGF-β1-induced lung cancer cell invasion and adhesion by targeting SOX7.
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miR-9通过靶向SOX7参与TGF-β1诱导的肺癌细胞侵袭和粘附。
DOI：
10.1111/jcmm.13120
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发表时间：
2017-09
影响因子：
5.3
通讯作者：
Zhang L
中科院分区：
文献类型：
--
作者：
Han L;Wang W;Ding W;Zhang L
microRNA（miR）-9在不同类型的癌症中发挥不同的作用。在此，我们研究了miR-9在体外非小细胞肺癌（NSCLC）细胞侵袭和粘附中的作用，并探讨了miR-9是否通过靶向SOX 7参与转化生长因子β 1（TGF-β1）诱导的NSCLC细胞侵袭和粘附。通过逆转录-定量聚合酶链反应检测人NSCLC组织和细胞系中miR-9和SOX 7的表达。在A549和HCC 827细胞上进行功能获得和功能丧失实验，以研究在存在或不存在TGF-β1的情况下miR-9和SOX 7对NSCLC细胞侵袭和粘附的影响。Transwell-Matrigel法和细胞粘附法检测细胞侵袭和粘附能力。进行荧光素酶报告基因测定以确定S 0X 7是否是miR-9的直接靶标。我们发现miR-9在人NSCLC组织和细胞系中上调，SOX 7下调。此外，SOX 7表达与miR-9表达呈负相关。miR-9敲低或SOX 7过表达可抑制TGF-β1诱导的NSCLC细胞侵袭和粘附。miR-9直接靶向SOX 7的3′非翻译区，并且SOX 7蛋白表达被miR-9下调。TGF-β1诱导NSCLC细胞中的miR-9表达。miR-9上调导致NSCLC细胞侵袭和粘附增强;然而，这些作用可通过SOX 7过表达减弱。我们得出结论，在人类NSCLC中，miR-9表达与SOX 7表达呈负相关。miR-9受TGF-β1上调，并通过直接靶向SOX 7促进TGF-β1诱导的NSCLC细胞侵袭和粘附。
MicroRNA (miR)‐9 plays different roles in different cancer types. Here, we investigated the role of miR‐9 in non‐small‐cell lung cancer (NSCLC) cell invasion and adhesion in vitro and explored whether miR‐9 was involved in transforming growth factor‐beta 1 (TGF‐β1)‐induced NSCLC cell invasion and adhesion by targeting SOX7. The expression of miR‐9 and SOX7 in human NSCLC tissues and cell lines was examined by reverse transcription‐quantitative polymerase chain reaction. Gain‐of‐function and loss‐of‐function experiments were performed on A549 and HCC827 cells to investigate the effect of miR‐9 and SOX7 on NSCLC cell invasion and adhesion in the presence or absence of TGF‐β1. Transwell–Matrigel assay and cell adhesion assay were used to examine cell invasion and adhesion abilities. Luciferase reporter assay was performed to determine whether SOX7 was a direct target of miR‐9. We found miR‐9 was up‐regulated and SOX7 was down‐regulated in human NSCLC tissues and cell lines. Moreover, SOX7 expression was negatively correlated with miR‐9 expression. miR‐9 knockdown or SOX7 overexpression could suppress TGF‐β1‐induced NSCLC cell invasion and adhesion. miR‐9 directly targets the 3′ untranslated region of SOX7, and SOX7 protein expression was down‐regulated by miR‐9. TGF‐β1 induced miR‐9 expression in NSCLC cells. miR‐9 up‐regulation led to enhanced NSCLC cell invasion and adhesion; however, these effects could be attenuated by SOX7 overexpression. We concluded that miR‐9 expression was negatively correlated with SOX7 expression in human NSCLC. miR‐9 was up‐regulated by TGF‐β1 and contributed to TGF‐β1‐induced NSCLC cell invasion and adhesion by directly targeting SOX7.
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影响因子：
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DOI：
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