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首页> 外文期刊>Journal of Cellular Physiology >GRP78 mediates cell growth and invasiveness in endometrial cancer
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GRP78 mediates cell growth and invasiveness in endometrial cancer

机译：GRP78介导细胞生长和侵袭性子宫内膜癌

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摘要

Recent studies have indicated that endoplasmic reticulum stress, the unfolded protein response activation and altered GRP78 expression can play an important role in a variety of tumors development and progression. Very recently we reported for the first time that GRP78 is increased in endometrial tumors. However, whether GRP78 could play a role in the growth and/or invasiveness of endometrial cancer cells is still unknown. Here we report that the silencing of GRP78 expression affects both cell growth and invasiveness of Ishikawa and AN3CA cells, analyzed by the (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and transwell migration assay, respectively. At variance with Ishikawa cells, AN3CA cells showed, besides an endoplasmic reticulum, also a plasma membrane GRP78 localization, evidenced by both immunofluorescence and cell membrane biotinylation experiments. Intriguingly, flow cytometry experiments showed that the treatment with a specific antibody targeting GRP78 C-terminal domain caused apoptosis in AN3CA but not in Ishikawa cells. Induction of apoptosis in AN3CA cells was not mediated by the p53 pathway activation but was rather associated to reduced AKT phosphorylation. Interestingly, immunofluorescence analysis evidenced that endometrioid adenocarcinoma tissues displayed, similarly to AN3CA cells, also a GRP78 plasma membrane localization. These data suggest that GRP78 and its plasma membrane localization, might play a role in endometrial cancer development and progression and might constitute a novel target for the treatment of endometrial cancer.
机译：最近的研究表明,内质的网压力,展开的蛋白质反应激活和改变GRP78的表达一个重要的角色在各种肿瘤开发和发展。首次报道,GRP78增加了子宫内膜肿瘤。GRP78可能发挥作用和/或增长子宫内膜癌细胞的侵袭性未知的。GRP78的表达影响细胞生长和石川和AN3CA细胞的侵袭性,分析(3 - (4, 5-dimethylthiazol-2-yl) 2, 5-diphenyl溴化四唑)和transwell迁移分别测定。细胞,AN3CA细胞显示,除了内质网,质膜GRP78本地化,都证明了这一点免疫荧光和细胞膜生物素酰化实验。血细胞计数实验表明,治疗与一个特定的抗体针对GRP78c端域在AN3CA但引起细胞凋亡不是在石川细胞。AN3CA不是由p53通路介导的细胞激活但相当减少有关一种蛋白激酶磷酸化。免疫荧光分析证明,endometrioid腺癌组织显示,类似于AN3CA细胞,GRP78等离子体膜定位。GRP78和质膜定位,可以在子宫内膜癌的发展和发挥的作用进展和可能构成小说的目标子宫内膜癌的治疗。

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