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克洛特里马通过破坏PI3K/AKT/mTOR通路来逆转巨细胞M2极化

José Xavier do Nascimento Júnior¹, Mauro Sola-Penna¹, Patricia Zancan¹

¹The MetaboliZSm GrouP, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.

Biochemical and biophysical research communications

|January 4, 2024

概括

克洛特里马 (CTZ) 通过抑制PI3K/AKT/mTOR通路,抑制NFkB信号传递,从而逆转M2巨细胞极化. 这一发现将CTZ定位为一种潜在的抗瘤剂,因为它准了原瘤M2巨细胞.

科学领域:

免疫学免疫学免疫学
癌症生物学癌症生物学
药理学药理学是指药理学的学科.

背景情况:

巨细胞表现出不同的激活状态,包括亲炎性 (M1) 和替代性/溶解性 (M2) 现型,这对疾病过程至关重要.
瘤微环境中的M2巨细胞促进瘤的进展和免疫逃避,使它们成为治疗点.
已知PI3K/AKT/mTOR通路抑制剂克洛特里马 (CTZ) 之前已经显示出抗瘤作用.

研究的目的:

调查CTZ影响巨细胞两极化的机制.
确定CTZ是否可以逆转M2巨细胞极化及其对信号通路的影响.
评估CTZ作为针对M2巨细胞的抗瘤治疗剂的潜力.

主要方法:

巨细胞被偏向到M2表型.
评估了CTZ对M2激活标记和M1极化标记的影响.
在CTZ治疗后分析了PI3K/AKT/mTOR信号通路中间体和NFkB通路组件.

主要成果:

CTZ显著降低了M2激活标志物的调节,但没有影响M1标志物或促炎细胞因子.
CTZ破坏了PI3K/AKT/mTOR信号传输,并抑制了NFkB路径中间体.
CTZ治疗逆转了M2巨细胞两极分化,表明从亲瘤起源的表型转移.

结论:

通过抑制PI3K/AKT/mTOR通路,CTZ有效地逆转M2巨细胞的两极分化.
这种逆转机制涉及抑制NFkB诱导M2极化.
通过调节瘤微环境中的巨细胞表型,CTZ显示出作为抗瘤剂的前景.

关键词:

炎症炎症是一种炎症.在M2中,极化为M2.通过PI3K路径.

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PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...