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首页> 外文期刊>Cell cycle >The RUNX1 transcription factor is expressed in serous epithelial ovarian carcinoma and contributes to cell proliferation, migration and invasion
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The RUNX1 transcription factor is expressed in serous epithelial ovarian carcinoma and contributes to cell proliferation, migration and invasion

机译：RUNX1转录因子在浆液性上皮性卵巢癌中表达，并有助于细胞增殖，迁移和侵袭

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Previously, we have identified the RUNX1 gene as hypomethylated and overexpressed in post-chemotherapy (CT) primary cultures derived from epithelial ovarian cancer (EO C) patients, when compared with primary cultures derived from matched primary (prior to CT) tumors. Here we show that RUNX1 displays a trend of hypomethylation, although not significant, in omental metastases compared with primary EO C tumors. Surprisingly, RUNX1 displayed significantly higher expression not only in metastatic tissue, but also in high-grade primary tumors and even in low malignant potential tumors. The RUNX1 expression levels were almost identical in primary tumors and omental metastases, suggesting that RUNX1 hypomethylation might have a limited impact on its overexpression in advanced (metastatic) stage of the disease. Knockdown of the RUNX1 expression in EO C cells led to sharp decrease of cell proliferation and induced G1 cell cycle arrest. Moreover, RUNX1 suppression significantly inhibited EO C cell migration and invasion. Gene expression profiling and consecutive network and pathway analyses confirmed these findings, as numerous genes and pathways known previously to be implicated in ovarian tumorigenesis, including EO C tumor invasion and metastasis, were found to be downregulated upon RUNX1 suppression, while a number of pro-apoptotic genes and some EO C tumor suppressor genes were induced. Taken together, our data are indicative for a strong oncogenic potential of the RUNX1 gene in EO C progression and suggest that RUNX1 might be a novel EO C therapeutic target. Further studies are needed to more completely elucidate the functional implications of RUNX1 and other members of the RUNX gene family in ovarian tumorigenesis.
机译：以前，与衍生自相匹配的原发性（CT之前）肿瘤的原发性培养物相比，我们已将RUNX1基因识别为低甲基化且在源自上皮性卵巢癌（EO C）患者的化疗后（CT）原发性培养物中过表达。在这里，我们显示与原发性EO C肿瘤相比，RUNX1在大网膜转移中显示低甲基化趋势，尽管不明显。出乎意料的是，RUNX1不仅在转移组织中而且在高度原发性肿瘤甚至低恶性潜能肿瘤中均显示出显着较高的表达。 RUNX1的表达水平在原发性肿瘤和网膜转移中几乎相同，这表明RUNX1的低甲基化可能在疾病的晚期（转移性）阶段对其过表达的影响有限。敲低EO C细胞中RUNX1表达的结果导致细胞增殖急剧下降并诱导G1细胞周期停滞。此外，RUNX1抑制显着抑制EO C细胞迁移和侵袭。基因表达谱分析以及连续的网络和途径分析证实了这些发现，因为先前已知与卵巢肿瘤发生有关的许多基因和途径（包括EO C肿瘤的侵袭和转移）在RUNX1抑制后均被下调，而许多诱导凋亡基因和一些EO C抑癌基因。综上所述，我们的数据表明RUNX1基因在EO C进展中具有强大的致癌潜力，并表明RUNX1可能是一种新型的EO C治疗靶标。需要更进一步的研究以更完全地阐明RUNX1和RUNX基因家族的其他成员在卵巢肿瘤发生中的功能含义。

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