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SCD‐KO cells are sensitive to acetylation inhibitors. (A) Proliferation assay with Incucyte at the indicated time points in control, SCD‐KO HT29 and MDA‐MB231 cells treated with DMSO (Ctrl) or a deacetylase inhibitor cocktail. (B) Cell proliferation assessment after 96 h of treatment. (C) Proliferation of cells treated with DMSO (Ctrl) or vorinostat (0.75 µM). (D) Cell proliferation assessment of cells treated as described in (C) at 96 h. (E) Tumor uptake table of MC38 mouse colorectal tumors on Day 7 and Day 17 post‐injection in C57/Bl6 mice with different treatments. (F) Growth of MC38 tumors in C57/Bl6 mice and treated with vehicle, vorinostat, or an SCD inhibitor (SCD1i) alone or with the combination of vorinostat and anti‐SCDi. (G) Tumor weights of MC38 tumors. (H) Growth of E0771 tumors <t>in</t> <t>C57BL/6</t> mice treated with vehicle, vorinostat, or an SCD inhibitor (SCD1i) alone or with a combination of vorinostat and SCD1i. (I) Growth of HT29 control (Ctrl) or PLIN2‐KO (PLIN2‐KO1) cells treated with vehicle or vorinostat. HT29 tumors were injected into RAG1 −/− mice ( n = 5). (J) Representative images of tumors from the experiment shown in (I). (K) Tumor weights of HT29 control and PLIN2‐KO cells treated with vehicle or vorinostat, corresponding to (I). ns: p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.
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SCD‐KO cells are sensitive to acetylation inhibitors. (A) Proliferation assay with Incucyte at the indicated time points in control, SCD‐KO HT29 and MDA‐MB231 cells treated with DMSO (Ctrl) or a deacetylase inhibitor cocktail. (B) Cell proliferation assessment after 96 h of treatment. (C) Proliferation of cells treated with DMSO (Ctrl) or vorinostat (0.75 µM). (D) Cell proliferation assessment of cells treated as described in (C) at 96 h. (E) Tumor uptake table of MC38 mouse colorectal tumors on Day 7 and Day 17 post‐injection in C57/Bl6 mice with different treatments. (F) Growth of MC38 tumors in C57/Bl6 mice and treated with vehicle, vorinostat, or an SCD inhibitor (SCD1i) alone or with the combination of vorinostat and anti‐SCDi. (G) Tumor weights of MC38 tumors. (H) Growth of E0771 tumors in C57BL/6 mice treated with vehicle, vorinostat, or an SCD inhibitor (SCD1i) alone or with a combination of vorinostat and SCD1i. (I) Growth of HT29 control (Ctrl) or PLIN2‐KO (PLIN2‐KO1) cells treated with vehicle or vorinostat. HT29 tumors were injected into RAG1 −/− mice ( n = 5). (J) Representative images of tumors from the experiment shown in (I). (K) Tumor weights of HT29 control and PLIN2‐KO cells treated with vehicle or vorinostat, corresponding to (I). ns: p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

Journal: MedComm

Article Title: Stearoyl‐CoA Desaturase‐1 Drives Tumor Growth by Interacting With Histone Deacetylase‐2 and Deacetylating Nucleophosmin‐1

doi: 10.1002/mco2.70809

Figure Lengend Snippet: SCD‐KO cells are sensitive to acetylation inhibitors. (A) Proliferation assay with Incucyte at the indicated time points in control, SCD‐KO HT29 and MDA‐MB231 cells treated with DMSO (Ctrl) or a deacetylase inhibitor cocktail. (B) Cell proliferation assessment after 96 h of treatment. (C) Proliferation of cells treated with DMSO (Ctrl) or vorinostat (0.75 µM). (D) Cell proliferation assessment of cells treated as described in (C) at 96 h. (E) Tumor uptake table of MC38 mouse colorectal tumors on Day 7 and Day 17 post‐injection in C57/Bl6 mice with different treatments. (F) Growth of MC38 tumors in C57/Bl6 mice and treated with vehicle, vorinostat, or an SCD inhibitor (SCD1i) alone or with the combination of vorinostat and anti‐SCDi. (G) Tumor weights of MC38 tumors. (H) Growth of E0771 tumors in C57BL/6 mice treated with vehicle, vorinostat, or an SCD inhibitor (SCD1i) alone or with a combination of vorinostat and SCD1i. (I) Growth of HT29 control (Ctrl) or PLIN2‐KO (PLIN2‐KO1) cells treated with vehicle or vorinostat. HT29 tumors were injected into RAG1 −/− mice ( n = 5). (J) Representative images of tumors from the experiment shown in (I). (K) Tumor weights of HT29 control and PLIN2‐KO cells treated with vehicle or vorinostat, corresponding to (I). ns: p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

Article Snippet: Syngeneic mouse tumors derived from MC38 or E0771 cells were generated in 6‐ to 8‐week‐old female C57BL/6 mice (Janvier).

Techniques: Proliferation Assay, Control, Histone Deacetylase Assay, Injection