Intracellular nutrients and the rate of energy lfowing in tumor cells are otfen higher than that in normal cells due to the prolonged stress of tumor-speciifc microenvironment. In this context, the metabolism of tumor cells provides the fuel of bio-synthesis and energy required for tumor metastasis. Consistent with this, the abnormal metabolism such as extremely active glucose metabolism and excessive accumulating of fatty acid is also discovered in metastatic tumors. Previous Studies have conifrmed that the regulation of tumor metabolism can affect the tumor metastasis, and some of these have been successfully applied in clinical effective, positive way. hTus, targeting metabolism of tumor cells might be an effectively positive way to prevent the metastasis of tumor. So, our review is focused on the research development of the relationship between tu-mor metabolism and metastasis as well as the underlying mechanism.

Background and objectivehTe CpG island aberrant promoter methylation in the tumor suppressor gene region plays an important role in the process of tumorigenesis. Relevant evidence shows that the promoter methylation of ARS association domain family 1A (ARSSF1A) gene, a tumor suppressor gene, has a close relationship with non-small cell lung cancer (NSCLC) development; therefore, ARSSF1A may be a potential NSCLC biomarker. hTis paper discussed and summa-rized the relationship betweenARSSF1A gene promoter methylation frequency and NSCLC throughmeta-analysis.Methods By searching Medline, EMBASE, CNKI, and Wanfang database, we selected and collected the published articles regarding RASSF1A gene promoter methylation and NSCLC risk according to the marked inclusion and exclusion criteria. Through meta-analysis, combined odds ratio (OR) and 95% confidence interval (CI) data were used to analyze theRASSF1A gene promoter methylation and NSCLC relationship.Results A total of 23 articles were utilized in this study. Results indicated that theARSSF1A gene promoter methylation rate was 41.50% (95%CI: 34%-49%) in NSCLC tissue and was 5.58% (95%CI: 2%-9%) for the control group. Compared with normal lung tissue, ARSSF1A methylation frequency in tumor tissue was sig-niifcantly higher than that of the control group (OR=8.72, 95%CI: 4.88-15.58,P<0.05). Subgroup analysis showed that the ARSSF1A gene promoter methylation rate of tumor tissue was higher than that of plasma group (OR=10.99, 95%CI: 2.48-48.68) and normal control tissue group (OR=8.74, 95%CI: 4.39-17.41).ConclusionhTe rate ofARSSF1A promoter gene methyla-tion in NSCLC patient tissue samples was higher than that of normal lung samples, whereas the rate ofARSSF1A promoter gene methylation in the tissue has more signiifcant effect on lung cancer occurrence. hTis ifnding indicates thatARSSF1A gene promoter methylation could be used as an NSCLC biomarker and was involved in NSCLC carcinogenic effects.