IGF2BP3 enhances lipid metabolism in cervical cancer by upregulating SCD expression. This study reveals that IGF2BP3 is highly expressed in cervical cancer (CC) tissues compared to adjacent normal tissues and is positively correlated with tumor stage. IGF2BP3 promotes CC cell proliferation, metastasis, and lipid metabolism by regulating SCD through N6-methyladenosine (m6A) modification via the IGF2BP3-METTL14 complex. SCD, a key enzyme in fatty acid metabolism, is a downstream target of IGF2BP3. Knockdown of IGF2BP3 in CC cells significantly reduces cell viability, colony formation, and lipid metabolism, while overexpression of SCD rescues these effects in vitro and in vivo. The study demonstrates that IGF2BP3 enhances SCD mRNA stability and translation, thereby promoting lipid metabolism and tumor progression. These findings highlight the role of IGF2BP3 in CC progression and suggest that targeting the IGF2BP3-SCD-lipid metabolism axis could be a potential therapeutic strategy for CC treatment. The results provide new insights into the molecular mechanisms underlying CC development and offer a promising approach for therapeutic intervention.IGF2BP3 enhances lipid metabolism in cervical cancer by upregulating SCD expression. This study reveals that IGF2BP3 is highly expressed in cervical cancer (CC) tissues compared to adjacent normal tissues and is positively correlated with tumor stage. IGF2BP3 promotes CC cell proliferation, metastasis, and lipid metabolism by regulating SCD through N6-methyladenosine (m6A) modification via the IGF2BP3-METTL14 complex. SCD, a key enzyme in fatty acid metabolism, is a downstream target of IGF2BP3. Knockdown of IGF2BP3 in CC cells significantly reduces cell viability, colony formation, and lipid metabolism, while overexpression of SCD rescues these effects in vitro and in vivo. The study demonstrates that IGF2BP3 enhances SCD mRNA stability and translation, thereby promoting lipid metabolism and tumor progression. These findings highlight the role of IGF2BP3 in CC progression and suggest that targeting the IGF2BP3-SCD-lipid metabolism axis could be a potential therapeutic strategy for CC treatment. The results provide new insights into the molecular mechanisms underlying CC development and offer a promising approach for therapeutic intervention.