Metastasis　accounts　for　the　majority　of　cancer-related　mortalities,　and　the　complex　processes　of　metastasis　remain　the　least　understood　aspect　of　cancer　biology.　Metabolic　reprogramming　is　associated　with　cancer　cell　survival　and　metastasis　in　a　hostile　envi　ronment　with　a　limited　nutrient　supply,　such　as　solid　tumors.　Little　is　known　regarding　the　differences　of　bioenergetic　adaptation　between　primary　tumor　cells　and　metastatic　tumor　cells　in　unfavorable　microenvironments;　to　clarify　these　differences,　the　present　study　aimed　to　compare　metabolic　reprogramming　of　primary　tumor　cells　and　metastatic　tumor　cells.　SW620　metastatic　tumor　cells　exhibited　stronger　bioenergetic　adaptation　in　unfavorable　conditions　compared　with　SW480　primary　tumor-derived　cells,　as　determined　by　the　sustained　elevation　of　glycolysis　and　regulation　of　the　cell　cycle.　This　remarkable　glycolytic　ability　of　SW620　cells　was　associated　with　high　expression　levels　of　hexokinase　(HK)1,　HK2,　glucose　transporter　type　1　and　hypoxia-inducible　factor　1　alpha.　Compared　with　SW480　cells,　the　expression　of　cell　cycle　regulatory　proteins　was　effectively　inhibited　in　SW620　cells　to　sustain　cell　survival　when　there　was　a　lack　of　energy.　Furthermore,　SW620　cells　exhibited　a　stronger　mesenchymal　phenotype　and　stem　cell　characteristics　compared　with　SW480　cells;　CD133　and　CD166　were　highly　expressed　in　SW620　cells,　whereas　expression　was　not　detected　in　SW480　cells.　These　data　may　explain　why　metastatic　cancer　cells　exhibit　greater　microenvironmental　adaptability　and　survivability;　specifically,　this　may　be　achieved　by　upregulating　glycolysis,　optimizing　the　cell　cycle　and　reprogramming　cell　metabolism.　The　present　study　may　provide　a　target　metabolic　pathway　for　cancer　metastasis　therapy.