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Desaturases such as stearoyl\u2010CoA desaturase (SCD) and fatty acid desaturase 2 (FADS2) have been implicated in multiple cancers, and their dominant and compensatory effects have recently been highlighted. However, how tumors initiate and sustain their self\u2010sufficient FA desaturation to maintain phenotypic transition remains elusive. This study aimed to explore the molecular orchestration of SCD and FADS2 and their specific reprogramming mechanisms in response to cancer progression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">The potential interactions between SCD and FADS2 were explored by bioinformatics analyses across multiple cancer cohorts, which guided subsequent functional and mechanistic investigations. The expression levels of desaturases were investigated with online datasets and validated in both cancer tissues and cell lines. Specific desaturation activities were characterized through various isomer\u2010resolved lipidomics methods and sensitivity assays using desaturase inhibitors. In\u2010situ lipid profiling was conducted using multiplex stimulated Raman scattering imaging. Functional assays were performed both in vitro and in vivo, with RNA\u2010sequencing employed for the mechanism verification.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">After integration of the RNA\u2010protein\u2010metabolite levels, the data revealed that a reprogramming from SCD\u2010dependent to FADS2\u2010dependent desaturation was linked to cancer epithelial\u2010mesenchymal transition (EMT) and progression in both patients and cell lines. FADS2 overexpression and SCD suppression concurrently maintained EMT plasticity. A FADS2\/\u03b2\u2010catenin self\u2010reinforcing feedback loop facilitated the degree of lipid unsaturation, membrane fluidity, metastatic potential and EMT signaling. Moreover, SCD inhibition triggered a lethal apoptosis but boosted survival plasticity by inducing EMT and enhancing FA uptake via adenosine monophosphate\u2010activated protein kinase activation. Notably, this desaturation reprogramming increased transforming growth factor\u2010\u03b22, effectively sustaining aggressive phenotypes and metabolic plasticity during EMT.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">These findings revealed a metabolic reprogramming from SCD\u2010dependent to FADS2\u2010dependent desaturation during cancer EMT and progression, which concurrently supports EMT plasticity. Targeting desaturation reprogramming represents a potential vulnerability for cancer metabolic therapy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cac2.12644","type":"journal-article","created":{"date-parts":[[2024,12,25]],"date-time":"2024-12-25T23:51:19Z","timestamp":1735170679000},"page":"245-280","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Orchestrated desaturation reprogramming from stearoyl\u2010CoA desaturase to fatty acid desaturase 2 in cancer epithelial\u2010mesenchymal transition and metastasis"],"prefix":"10.34133","volume":"45","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7549-4696","authenticated-orcid":false,"given":"Zhicong","family":"Chen","sequence":"first","affiliation":[{"name":"The Third Affiliated Hospital","place":["Guangzhou, P. R. China"]},{"name":"Guangzhou Medical University","place":["Guangzhou, P. R. 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