Additional file 1 of Pharmacological induction of membrane lipid poly-unsaturation sensitizes melanoma to ROS inducers and overcomes acquired resistance to targeted therapy
Creators: name: Talebi, Ali
name: de Laat, Vincent
name: Spotbeen, Xander
name: Dehairs, Jonas
name: Rambow, Florian
name: Rogiers, Aljosja
name: Vanderhoydonc, Frank
name: Rizotto, Lara
name: Planque, Mélanie
name: Doglioni, Ginevra
name: Motamedi, Sahar
name: Nittner, David
name: Roskams, Tania
name: Agostinis, Patrizia
name: Bechter, Oliver
name: Boecxstaens, Veerle
name: Garmyn, Marjan
name: O’Farrell, Marie
name: Wagman, Alan
name: Kemble, George
name: Leucci, Eleonora
name: Fendt, Sarah-Maria
name: Marine, Jean-Christophe
name: Swinnen, Johannes V.
Publisher: name: figshare
Year: 2023
Subjects: subject: Biochemistry
subject: Space Science
subject: Medicine
subject: Cell Biology
subject: Genetics
subject: FOS: Biological sciences
subject: Pharmacology
subject: Biotechnology
subject: 39999 Chemical Sciences not elsewhere classified
subject: FOS: Chemical sciences
subject: Cancer
subject: Hematology
subject: 110309 Infectious Diseases
subject: FOS: Health sciences
subject: 60506 Virology

description: Additional file 1: Supplementary Figure S1. Lipogenic gene expression is associated with resistance to MAPKi therapy. Supplementary Figure S2. FASN and MAPK inhibition affect lipogenesis and lipid uptake. Supplementary Figure S3. Lipogenesis inhibition cooperates with MAPK inhibition to reduce cell proliferation. Supplementary Figure S4. ACACA and FASN knockdown cooperate with MAPK inhibition to reduce cell proliferation. Supplementary Figure S5. Lipogenesis inhibition cooperates with MAPK inhibition to reduce cell proliferation in BRAF wild-type cells. Supplementary Figure S6. MAPK inhibition response in Mel006 tumors is associated with membrane lipid polyunsaturation. Supplementary Figure S7. MAPK inhibition and FASN inhibition drive membrane polyunsaturation in D10 BMR cells. Supplementary Figure S8. MAPK inhibition and FASN inhibition increase membrane disorder in 451lu R and D10 BMR cells. Supplementary Figure S9. Phospholipidomics alterations following FASN and MAPK inhibition can be modulated by exogenous fatty acid supplementation in 451lu R. Supplementary Figure S10. Proliferation following FASN and MAPK inhibition can be modulated by exogenous fatty acid supplementation in D10 BMR cells. Supplementary Figure S11. Piperazine erastin and RSL3 sensitize D10 BMR cells to FASN and MAPK inhibition. Supplementary Figure S12. A host of ROS elevating compounds sensitize D10 BMR cells to FASN and MAPK inhibition. Supplementary Figure S13. Treatment combinations do not significantly alter mitochondrial membrane potential in 451lu R D10 BMR cells. Supplementary Figure S14. Exogenous fatty acid supplementation modulates the sensitivity of D10 BMR cells to FASN and MAPK inhibition in combination with ATO exposure. Supplementary Figure S15. Ferrostatin-1 but not ZVAD modulates the sensitivity of D10 BMR cells to FASN and MAPK inhibition in combination with ATO exposure. Supplementary Figure S16. The combination of FASN and MAPK inhibition with ATO treatment increases progression-free survival in Mel006 tumor bearing mice.