原句:Involvement of the pro-oncogenic enzyme fatty acid synthase in the hallmarks of cancer: a promising target in anti-cancer therapies. 简化汉语:脂肪酸合酶作为一个增癌基因酶,在癌症标志物中起到作用:是抗癌治疗中值得期待的一个目标。
Involvement of the pro-oncogenic enzyme fatty acid synthase in the hallmarks of cancer: a promising target in anti-cancer therapies.
发表日期:2023 Mar 18
作者:
Dimitri Vanauberg, Céline Schulz, Tony Lefebvre
来源:
Cell Death & Disease
摘要:
快速的脂质新生(DNL)通量是癌细胞的一个共同特征,它需要维持高度增殖率。DNL酶脂肪酸合酶(FASN)在许多癌症中过度表达,是增加脂肪酸生产的关键。越来越多的证据表明,FASN涉及癌症的几个标志性特征,与其通过膜生物合成促进细胞增殖的能力有关。在这篇综述中,我们将讨论FASN在耐受细胞死亡和通过增加核酸、蛋白质和脂质合成来调节细胞能量方面的作用。FASN还通过使脂质浮岛建造成为可能,在膜微区定位致癌受体例如HER2和c-Met,促进细胞增殖、侵袭、转移和血管生成。最后,FASN通过抑制炎性细胞的激活,促进M2巨噬细胞和T调节细胞在肿瘤微环境中的招募,参与免疫逃逸。在这里,我们提供了一个关于这种促癌酶在癌症标志特征中的涉及的概述,使得FASN成为抗癌治疗中一种有前途的靶点,以克服耐受化疗的问题。©2023.作者(S)。
An accelerated de novo lipogenesis (DNL) flux is a common characteristic of cancer cells required to sustain a high proliferation rate. The DNL enzyme fatty acid synthase (FASN) is overexpressed in many cancers and is pivotal for the increased production of fatty acids. There is increasing evidences of the involvement of FASN in several hallmarks of cancer linked to its ability to promote cell proliferation via membranes biosynthesis. In this review we discuss about the implication of FASN in the resistance to cell death and in the deregulation of cellular energetics by increasing nucleic acids, protein and lipid synthesis. FASN also promotes cell proliferation, cell invasion, metastasis and angiogenesis by enabling the building of lipid rafts and consequently to the localization of oncogenic receptors such as HER2 and c-Met in membrane microdomains. Finally, FASN is involved in immune escape by repressing the activation of pro-inflammatory cells and promoting the recruitment of M2 macrophages and T regulatory cells in the tumor microenvironment. Here, we provide an overview of the involvement of the pro-oncogenic enzyme in the hallmarks of cancer making FASN a promising target in anti-cancer therapy to circumvent resistance to chemotherapies.© 2023. The Author(s).