The functional analysis of lipocalin2 and novel molecular targeted therapy for endometrial carcinoma

在过表达LCN2的子宫内膜癌细胞株HHUA中，利用shRNA抑制脂脂化蛋白2 （lipocalin2, LCN2）的表达。经紫外光（UV）或顺铂（CDDP）处理后，lcn2沉默的HHUA细胞活力显著降低，凋亡细胞显著增加。铁螯合也降低了细胞活力，类似于lcn2抑制。在lcn2沉默的HHUA中，磷酸化Akt的表达降低。这些发现表明LCN2通过铁和Akt磷酸化提高细胞存活。

The expression of lipocalin2 (LCN2) was silenced using shRNA in HHUA, an endometrial carcinoma cell line over-expressing LCN2. The cell viability was significantly reduced and the apoptotic cells were significantly increased in this LCN2-silenced HHUA after ultraviolet (UV) irradiation or cisplatin (CDDP) treatment. The iron-chelating also reduced cell viability similar to LCN2-suppression. The expression of phosphorylated Akt was reduced in LCN2-silenced HHUA. These findings suggested that LCN2 enhanced cell survival via iron and Akt phosphorylation.