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.

加速从头脂肪生成 (DNL) 通量是维持高增殖率所需的癌细胞的共同特征。DNL 酶脂肪酸合酶 (FASN) 在许多癌症中过度表达，并且对于增加脂肪酸的产生至关重要。越来越多的证据表明 FASN 参与了几个癌症标志，这些标志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，我们讨论了 FASN 在抵抗细胞死亡和通过增加核酸、蛋白质和脂质合成来放松细胞能量学方面的意义。FASN 还促进细胞增殖、细胞侵袭、转移和血管生成，通过建立脂筏，从而定位膜微区中的致癌受体，如 HER2 和 c-Met。最后，FASN 通过抑制促炎细胞的激活和促进​​肿瘤微环境中 M2 巨噬细胞和 T 调节细胞的募集参与免疫逃逸。在这里，我们概述了促癌酶参与癌症的标志，使 FASN 成为抗癌治疗中有希望的靶标，以规避对化学疗法的耐药性。