Journal: Cancer Research

Article Title: DGAT1 Inhibition Induces Ferroptosis and Enhances Cancer Immunotherapy Efficacy

doi: 10.1158/0008-5472.CAN-25-0840

Figure Lengend Snippet: LD reduction induces lipid peroxidation and mitochondrial dysfunction in DGAT1-deficient cells. A–C, Representative immunofluorescence images ( A ) and relative integrated intensities of LD staining ( B and C ) in control and DGAT1- KO or pradigastat-treated B16F10 cells. Scale bars, 25 µm. D and E, Quantification of MDA levels in control and DGAT1-KO ( D ) or pradigastat-treated ( E ) B16F10 cells. F–J, Levels of TG ( F ), DHA-cholesteryl ester (DHA-CE) 22:6 ( G ), HexCer d18:2/20:0 ( H ), HexCer d18:2/22:0 ( I ), and HexCer d18:2/23:0 ( J ) in control and DGAT1-KO B16F10 cells. K–M, JC-1 dye staining showing representative immunofluorescence images of MMP ( K ) and monomer/aggregate ratios in control ( L ), DGAT1- KO ( M ), or pradigastat-treated B16F10 cells. Scale bars, 25 µm. N and O, Flow cytometry analysis of ROS levels ( N ) and mean fluorescence intensity (MFI; O ) in control and DGAT1- KO B16F10 cells. P and Q, Flow cytometry analysis of ROS levels ( P ) and MFI ( Q ) in control and pradigastat-treated B16F10 cells. R and S, Representative immunofluorescence images ( R ) and relative integrated intensities of LD staining ( S ) in control and triacsin C–treated B16F10 cells. Scale bars, 25 µm. T, Quantification of MDA levels in control and triacsin C–treated B16F10 cells. U and V, Flow cytometry analysis of ROS levels ( U ) and mean fluorescence intensity ( V ) in control and triacsin C–treated B16F10 cells. Error bars represent ±SEM throughout the figure. P values were calculated using an unpaired t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001. VC, vector control.

Article Snippet: Triacsin C (2 μmol/L; MCE, cat. #HY-N6707) was administered to cells for 48 hours to induce the LDs.

Techniques: Immunofluorescence, Staining, Control, Flow Cytometry, Fluorescence, Plasmid Preparation

Journal: Cancer Research

Article Title: DGAT1 Inhibition Induces Ferroptosis and Enhances Cancer Immunotherapy Efficacy

doi: 10.1158/0008-5472.CAN-25-0840

Figure Lengend Snippet: DGAT1 deficiency induces GPX4 depletion and a ferroptosis phenotype. A–D, Quantification of GSH levels in control and DGAT1- KO or pradigastat-treated B16F10 ( A and B ) and A375 ( C and D ) cells. E, Quantification of GSH levels in control and triacsin C–treated B16F10 cells. F, Representative TEM images of mitochondria in control and DGAT1-KO or pradigastat-treated B16F10 cells. Scale bars, 0.5 µm. G and H, Western blot analysis of GPX4 expression in control and DGAT1- KO or pradigastat-treated B16F10 ( G ) and A375 ( H ) cells. I and J, Representative TEM images of mitochondria in control and DGAT1-KO ( I ) or pradigastat-treated ( J ) B16F10 cells combined with Fer-1 treatment. Scale bars, 0.5 µm. K and L, Western blot analysis of GPX4 levels in control and DGAT1- KO ( K ) or pradigastat-treated ( L ) B16F10 cells combined with Fer-1 treatment. M and N, Tumor growth delay ( M ) and Kaplan–Meier survival curves ( N ) in C57BL/6 mice inoculated subcutaneously with 1 × 10 5 DGAT1- KO B16F10 cells and treated with Fer-1 and anti–PD-1 antibody or isotype control. O, Quantification of MDA levels in control, DGAT1- KO, RSL3, and DGAT1-KO combined RSL3-treated B16F10 cells. P and Q, Tumor growth delay ( P ) and Kaplan–Meier survival curves ( Q ) in C57BL/6 mice inoculated subcutaneously with 1 × 10 5 DGAT1- KO B16F10 cells and treated with RSL3 and anti–PD-1 antibody or isotype control. Error bars represent ±SEM throughout the figure. P values were determined by unpaired t test ( A–E and O ), two-way ANOVA ( M and P ), and log-rank test ( N and Q ), respectively. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant. VC, vector control.

Article Snippet: Triacsin C (2 μmol/L; MCE, cat. #HY-N6707) was administered to cells for 48 hours to induce the LDs.

Techniques: Control, Western Blot, Expressing, Plasmid Preparation