Cancer cells reprogram their fatty acid metabolism to support growth, division, and survival. Fatty acids (FAs) are essential for membrane structure, signaling, and energy production. This review explores how cancer cells alter FA metabolism, focusing on four areas: (1) de novo synthesis and exogenous uptake of FAs, (2) regulation of FA metabolism by oncogenic pathways like PI3K-AKT-mTOR, (3) roles of FAs in cancer progression and metastasis, and (4) therapeutic strategies targeting FA metabolism. FAs are obtained through exogenous uptake via transporters like CD36, FATPs, and FABPpm, or de novo synthesis from glucose, glutamine, and acetate. Cancer cells preferentially take up FAs from adipose tissue, which supports metastasis by enhancing FA availability and activating pathways like AMPK. Excess FAs are stored in lipid droplets (LDs), which provide energy and NADPH during metabolic stress. β-oxidation of LDs generates ATP and NADPH, crucial for cancer cell survival. FAs also contribute to tumor microenvironment remodeling, promoting inflammation and angiogenesis. Dysregulated FA metabolism is linked to poor prognosis, and targeting FA metabolism is a promising therapeutic approach. Oncogenic signaling pathways, such as PI3K-AKT-mTOR, regulate FA metabolism by modulating enzymes involved in lipogenesis, β-oxidation, and lipid storage. FASN, a key enzyme in FA synthesis, is upregulated in many cancers and is involved in tumor progression. FASN also interacts with other signaling pathways, such as MAPK-ERK and PI3K-AKT, influencing cancer cell behavior. Inhibiting FASN can reduce tumor growth and enhance the effects of other therapies. The interplay between FA metabolism and oncogenic signaling is complex, and understanding these interactions is crucial for developing effective cancer therapies.Cancer cells reprogram their fatty acid metabolism to support growth, division, and survival. Fatty acids (FAs) are essential for membrane structure, signaling, and energy production. This review explores how cancer cells alter FA metabolism, focusing on four areas: (1) de novo synthesis and exogenous uptake of FAs, (2) regulation of FA metabolism by oncogenic pathways like PI3K-AKT-mTOR, (3) roles of FAs in cancer progression and metastasis, and (4) therapeutic strategies targeting FA metabolism. FAs are obtained through exogenous uptake via transporters like CD36, FATPs, and FABPpm, or de novo synthesis from glucose, glutamine, and acetate. Cancer cells preferentially take up FAs from adipose tissue, which supports metastasis by enhancing FA availability and activating pathways like AMPK. Excess FAs are stored in lipid droplets (LDs), which provide energy and NADPH during metabolic stress. β-oxidation of LDs generates ATP and NADPH, crucial for cancer cell survival. FAs also contribute to tumor microenvironment remodeling, promoting inflammation and angiogenesis. Dysregulated FA metabolism is linked to poor prognosis, and targeting FA metabolism is a promising therapeutic approach. Oncogenic signaling pathways, such as PI3K-AKT-mTOR, regulate FA metabolism by modulating enzymes involved in lipogenesis, β-oxidation, and lipid storage. FASN, a key enzyme in FA synthesis, is upregulated in many cancers and is involved in tumor progression. FASN also interacts with other signaling pathways, such as MAPK-ERK and PI3K-AKT, influencing cancer cell behavior. Inhibiting FASN can reduce tumor growth and enhance the effects of other therapies. The interplay between FA metabolism and oncogenic signaling is complex, and understanding these interactions is crucial for developing effective cancer therapies.