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镓试剂,一种Gβγ亚基信号抑制剂,可抑制表达OR51E2并暴露于其气味配体的肿瘤细胞的转移扩散。

Gallein, a Gβγ subunit signalling inhibitor, inhibits metastatic spread of tumour cells expressing OR51E2 and exposed to its odorant ligand.

作者信息

Sanz Guenhaël, Leray Isabelle, Muscat Adeline, Acquistapace Adrien, Cui Tao, Rivière Julie, Vincent-Naulleau Silvia, Giandomenico Valeria, Mir Lluis M

机构信息

NBO, INRA, Université Paris Saclay, 78350, Jouy-En-Josas, France.

Biologie du Développement et Reproduction, INRA, ENVA, Université Paris-Saclay, 78350, Jouy-En-Josas, France.

出版信息

BMC Res Notes. 2017 Oct 30;10(1):541. doi: 10.1186/s13104-017-2879-z.

Abstract

OBJECTIVE

We previously reported that the olfactory receptor OR51E2, overexpressed in LNCaP prostate cancer cells, promotes cell invasiveness upon stimulation of its agonist β-ionone, and this phenomenon increases metastatic spread. Furthermore, we showed that the induced cell invasiveness involves a PI3 kinase dependent signalling pathway. We report here the results of a new investigation to address whether gallein, a small inhibitor of G protein βγ subunit interaction with PI3 kinase, can inhibit β-ionone effects both in vitro and in vivo.

RESULTS

We demonstrate that gallein can inhibit the β-ionone-induced cell invasiveness in vitro, as well as the spread of metastases in vivo. LNCaP cell invasiveness, assessed using spheroid cultures in collagen gels in vitro, was increased by β-ionone and the effect was reversed by co-administration of gallein. LNCaP tumour cells, subcutaneously inoculated to immunodeficient mice, generated more metastases in vivo when β-ionone was applied through the skin. Furthermore, the intraperitoneal injection of gallein inhibited this increased metastasis spread. Our results thus support the role of OR51E2 in the β-ionone observed effects, and suggest that gallein could be a potential new agent in personalized medicine of the tumours expressing OR51E2.

摘要

目的

我们之前报道过,在LNCaP前列腺癌细胞中过表达的嗅觉受体OR51E2,在其激动剂β-紫罗兰酮刺激后会促进细胞侵袭,且这种现象会增加转移扩散。此外,我们还表明,诱导的细胞侵袭涉及PI3激酶依赖性信号通路。我们在此报告一项新研究的结果,以探讨小G蛋白βγ亚基与PI3激酶相互作用的抑制剂加兰他敏是否能在体外和体内抑制β-紫罗兰酮的作用。

结果

我们证明加兰他敏可以在体外抑制β-紫罗兰酮诱导的细胞侵袭以及在体内抑制转移扩散。使用体外胶原凝胶中的球体培养评估LNCaP细胞侵袭,β-紫罗兰酮会增加其侵袭,而加兰他敏共同给药可逆转这种作用。皮下接种到免疫缺陷小鼠的LNCaP肿瘤细胞,当通过皮肤应用β-紫罗兰酮时,在体内会产生更多转移灶。此外,腹腔注射加兰他敏可抑制这种增加的转移扩散。因此,我们的结果支持OR51E2在观察到的β-紫罗兰酮作用中的作用,并表明加兰他敏可能是表达OR51E2肿瘤个性化医疗中的一种潜在新药。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2d/5663063/31317ed7a013/13104_2017_2879_Fig1_HTML.jpg

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