## 1 Introduction  
Cancers are characterized by disordered metabolism. Specific metabolic activities essential to cell transformation or other related biological processes promote tumor growth [1, 2]. In order to meet the needs of both energy and biosynthesis, cancer cells can \"reprogram\" their metabolism systems mainly through the following mechanisms:  
(1) Increased uptake and utilization of nutrient substrates, especially glucose. In cancer cells, the glycolytic rate is approximately 30-fold higher than that in normal cells. Thus, the rate-limiting step in glucose metabolism is glucose uptake across the plasma membrane, which is carried out by glucose transporter 1 (GLUT1), a protein with an oncogenic role and frequent overexpression in cancer cells [3, 4];  
(2) Employing metabolic pathways beneficial to biosynthesis in the catabolism of nutrients. A well-cited example is the \"Warburg effect\" [5] that reveals the propensity of cancer cells to consume glucose through anaerobic glycolysis even under aerobic conditions. In terms of ATP production, glycolysis is inefficient compared to oxidative phosphorylation. Importantly, converting glucose into lactate instead of utilizing it through mitochondrial metabolism provides more substrates and thus permits the synthesis of various biomolecules, such as fatty acids and amino acids [5]. The pentose phosphate pathway (PPP) is another major pathway of glucose catabolism that produces important resources for biosynthesis, such as ribose 5-phosphate (R5P) and NADPH [6];(3) Aberrantly activated biosynthesis pathways. To meet the excessive demands of cell membranes and signaling molecules in tumors, a number of pathways related to fatty acid biosynthesis and their desaturation pathways in tumor cells are remarkably active. Fatty acid synthase (FASN), a key enzyme to catalyze the cellular process of fatty acid synthesis, exhibits oncogenic activity and is a bona fide target in cancer therapies [7]. \"Reprogrammed\" metabolic processes are not only important for cancer cell growth but also increasingly appreciated as a major determinant of cell destiny [8; 9]. Rapid proliferation is a key characteristic of cancer cells, which confers them with oncogene addiction and non-oncogene dependence, including metabolic dependence. This allows us to design effective strategies and develop new clinical anticancer agents [10]. Compared with synthetic chemicals, natural compounds have several advantages, such as decent safety, low side effects and multistep targeting; thus, many of them have been used as therapeutic and preventive agents for a number of diseases, including cancers. Various compounds from edible plants and traditional Chinese herbals have been revealed to have suppressive effects on the initiation, development and metastasis of human cancers [11; 12]. Some of these compounds with well-characterized anticancer activities, such as paclitaxel, are already in the clinic. Although a number of natural compounds have been used for many years and their anticancer characteristics are well-appreciated, the underlying molecular mechanisms of their tumor-suppressive action still remain elusive. To date, an increasing number of natural compounds have been demonstrated to block metabolic processes in cancer cells. Many of them can repress tumor growth through directly or indirectly regulating different rate-limiting enzymes, especially those involved in glucose and lipid metabolism [13; 14]. For example, GLUT1 is inhibited by multiple components in green tea extracts, and each compound exhibits unique characteristics to exert the activity, dependent on its specific structural feature and GLUT1-binding mode. In addition, as a key enzyme of lipid synthesis, FASN is blocked by many small molecule compounds through their binding to different functional domains. Comprehensively reviewing and comparing the existing research data can improve our understanding of anticancer mechanisms of natural small molecule compounds.