Understanding the connection between metabolic pathways and cancer is very important for the development of new therapeutic approaches based on regulatory enzymes in pathways associated with tumorigenesis. The mevalonate cascade and its rate-liming enzyme HMG CoA-reductase has recently drawn the attention of cancer researchers because strong evidences arising mostly from epidemiologic studies, show that it could promote transformation. Hence, these studies pinpoint HMG CoA-reductase as a candidate proto-oncogene. Several recent epidemiological studies, in different populations, have proven that statins are beneficial for the treatment-outcome of various cancers, and may improve common cancer therapy strategies involving alkylating agents, and antimetabolites. Cancer stem cells/cancer initiating cells (CSC) are key to cancer progression and metastasis. Therefore, in the current review we address the different effects of statins on cancer stem cells. The mevalonate cascade is among the most pleiotropic, and highly interconnected signaling pathways. Through G-protein-coupled receptors (GRCP), it integrates extra-, and intracellular signals. The mevalonate pathway is implicated in cell stemness, cell proliferation, and organ size regulation through the Hippo pathway (e.g. Yap/Taz signaling axis). This pathway is a prime preventive target through the administration of statins for the prophylaxis of obesity-related cardiovascular diseases. Its prominent role in regulation of cell growth and stemness also invokes its role in cancer development and progression. The mevalonate pathway affects cancer metastasis in several ways by: (i) affecting epithelial-to-mesenchymal transition (EMT), (ii) affecting remodeling of the cytoskeleton as well as cell motility, (iii) affecting cell polarity (non-canonical Wnt/planar pathway), and (iv) modulation of mesenchymal-to-epithelial transition (MET). Herein we provide an overview of the mevalonate signaling network. We then briefly highlight diverse functions of various elements of this mevalonate pathway. We further discuss in detail the role of elements of the mevalonate cascade in stemness, carcinogenesis, cancer progression, metastasis and maintenance of cancer stem cells.

了解新陈代谢途径与癌症之间的联系对于基于与肿瘤发生有关的途径中的调节酶的新治疗方法的开发非常重要。甲羟戊酸酯级联反应及其限速酶HMG CoA还原酶最近引起了癌症研究人员的关注，因为主要来自流行病学研究的有力证据表明，甲氧戊酸可以促进转化。因此，这些研究将HMG CoA还原酶确定为候选原癌基因。最近在不同人群中进行的几项流行病学研究证明，他汀类药物对多种癌症的治疗结果均有益，并且可以改善涉及烷基化剂和抗代谢物的常见癌症治疗策略。癌症干细胞/癌症起始细胞（CSC）是癌症进展和转移的关键。因此，在本综述中，我们探讨了他汀类药物对癌症干细胞的不同作用。甲羟戊酸酯级联是最具多效性和高度相互联系的信号传导途径之一。通过G蛋白偶联受体（GRCP），它整合了细胞外信号和细胞内信号。甲羟戊酸途径通过河马途径参与细胞干性，细胞增殖和器官大小调节（例如Yap / Taz信号轴）。通过服用他汀类药物预防肥胖相关的心血管疾病，该途径是主要的预防目标。它在调节细胞生长和干性中的重要作用也唤起了它在癌症发展和进程中的作用。甲羟戊酸途径通过以下几种方式影响癌症转移：（i）影响上皮到间充质转化（EMT），（ii）影响细胞骨架的重塑以及细胞运动，（iii）影响细胞极性（非经典Wnt /平面路径），以及（iv）调节间质到上皮的转化（MET）。在此，我们提供了甲羟戊酸信令网络的概述。然后，我们简要强调了该甲羟戊酸途径的各种元素的多种功能。