Tumor suppressors and cell metabolism: a recipe for cancer growth Tumor cells have altered metabolic pathways that result from oncogenic mutations. These changes are linked to metabolic regulation and help cancer cells survive under stress. Tumor suppressors play a critical role in suppressing growth and proliferation when essential metabolites are limited. The review discusses how oncogene and tumor suppressor networks influence cellular metabolism and bioenergetics to support growth and survival under metabolic stress. It also explores the implications of metabolic reprogramming for tumor growth and potential therapeutic strategies. Tumor cells must increase biomass and replicate their genome to divide. This requires sufficient energy and biosynthetic activity. Cancer cells often display fundamental changes in energy metabolism and nutrient uptake. The Warburg effect, where tumor cells prefer glycolysis over mitochondrial oxidative phosphorylation, is a key feature of cancer metabolism. This effect is exploited in clinical settings through FDG-PET imaging. The metabolic switch in cancer cells, known as metabolic transformation, provides a selective growth advantage and resistance to apoptosis. However, increased metabolic potential poses challenges for malignant cells. Tumors must adapt to maintain cellular bioenergetics. The review discusses how oncogenes and tumor suppressors influence cellular metabolism and bioenergetics to support growth and survival under metabolic stress. Glycolysis is a primary metabolic change in proliferating tumor cells. It provides energy and metabolic intermediates for cell growth. The enzyme PKM2 regulates the flux of carbon into nucleotide and fatty acid biosynthesis. The mitochondrion also plays a role in biosynthesis, converting metabolites into intermediates for other biosynthetic pathways. Tumor suppressors and oncogenes constitute metabolic signaling networks. The PI3K/Akt pathway is a central regulator of metabolism in both normal and transformed cells. It coordinates metabolic activities that support cellular biosynthesis. Tumor suppressors such as PTEN and TSC1/TSC2 regulate mTOR activity. The AMPK pathway is a key sensor of metabolic stress and regulates energy homeostasis. p53 is a transcription factor that functions in a complex signaling network to mediate cellular adaptation to stress. It can influence metabolic balance between glycolysis and OXPHOS. p53 activation can reinforce AMPK-dependent responses through feedback loops. The AMPK-p53 pathway is important for metabolic adaptation. Hypoxia, or reduced oxygen availability, stimulates metabolic adaptation in cells. Hypoxia-inducible factor 1 (HIF1) is a transcription factor complex activated by hypoxic stress. HIF1 promotes aerobic glycolysis and other metabolic adaptations. HIF1 activity is regulated by oxygen levels and other stress signals. Autophagy is a key metabolic stress response that functions as a tumor suppressor mechanism. It involves the sequestration of internal components and organelles into autophagic vesicles, followed by degradation by lysosomes. Autophagy can promote cell viability by providing energyTumor suppressors and cell metabolism: a recipe for cancer growth Tumor cells have altered metabolic pathways that result from oncogenic mutations. These changes are linked to metabolic regulation and help cancer cells survive under stress. Tumor suppressors play a critical role in suppressing growth and proliferation when essential metabolites are limited. The review discusses how oncogene and tumor suppressor networks influence cellular metabolism and bioenergetics to support growth and survival under metabolic stress. It also explores the implications of metabolic reprogramming for tumor growth and potential therapeutic strategies. Tumor cells must increase biomass and replicate their genome to divide. This requires sufficient energy and biosynthetic activity. Cancer cells often display fundamental changes in energy metabolism and nutrient uptake. The Warburg effect, where tumor cells prefer glycolysis over mitochondrial oxidative phosphorylation, is a key feature of cancer metabolism. This effect is exploited in clinical settings through FDG-PET imaging. The metabolic switch in cancer cells, known as metabolic transformation, provides a selective growth advantage and resistance to apoptosis. However, increased metabolic potential poses challenges for malignant cells. Tumors must adapt to maintain cellular bioenergetics. The review discusses how oncogenes and tumor suppressors influence cellular metabolism and bioenergetics to support growth and survival under metabolic stress. Glycolysis is a primary metabolic change in proliferating tumor cells. It provides energy and metabolic intermediates for cell growth. The enzyme PKM2 regulates the flux of carbon into nucleotide and fatty acid biosynthesis. The mitochondrion also plays a role in biosynthesis, converting metabolites into intermediates for other biosynthetic pathways. Tumor suppressors and oncogenes constitute metabolic signaling networks. The PI3K/Akt pathway is a central regulator of metabolism in both normal and transformed cells. It coordinates metabolic activities that support cellular biosynthesis. Tumor suppressors such as PTEN and TSC1/TSC2 regulate mTOR activity. The AMPK pathway is a key sensor of metabolic stress and regulates energy homeostasis. p53 is a transcription factor that functions in a complex signaling network to mediate cellular adaptation to stress. It can influence metabolic balance between glycolysis and OXPHOS. p53 activation can reinforce AMPK-dependent responses through feedback loops. The AMPK-p53 pathway is important for metabolic adaptation. Hypoxia, or reduced oxygen availability, stimulates metabolic adaptation in cells. Hypoxia-inducible factor 1 (HIF1) is a transcription factor complex activated by hypoxic stress. HIF1 promotes aerobic glycolysis and other metabolic adaptations. HIF1 activity is regulated by oxygen levels and other stress signals. Autophagy is a key metabolic stress response that functions as a tumor suppressor mechanism. It involves the sequestration of internal components and organelles into autophagic vesicles, followed by degradation by lysosomes. Autophagy can promote cell viability by providing energy