Fig. 4: SLC39A4 enhanced resistance to cuproptosis in GC cells. | Cancer Gene Therapy

Fig. 4: SLC39A4 enhanced resistance to cuproptosis in GC cells.

From: YTHDF1/SLC39A4 signaling axis promotes gastric cancer cell proliferation by suppressing cuproptosis ex vivo and in vitro

Fig. 4: SLC39A4 enhanced resistance to cuproptosis in GC cells.The alternative text for this image may have been generated using AI.

The GC cells were treated with 1 μM CuCl2 and different concentrations of elesclomol for 48 h. Cell survival rate in SLC39A4-overexpressed (A, B) and SLC39A4-silence (C, D) cells. Protein expression of cuproptosis markers FDX1 and Lip-DLAT in SLC39A4-overexpressed (E, F) and SLC39A4-silenced (G, H) cells. Representative oligomers-DLAT immunofluorescence staining images of SLC39A4-overexpressed (I) and SLC39A4-silenced (J) cells. N = 3. SLC39A4 Solute carrier family 39 member 4, GC gastric cancer, EC elesclomol, Cu copper, FDX1 ferredoxin 1, DLAT dihydrolipoamide S-acetyltransferase, Lip-DLAT lipoylation of dihydrolipoamide S-acetyltransferase, DAPI 4’, 6-diamidino-2-phenylindole, NC-Sh negative control short hairpin RNA sequence, shSLC39A4-KD-11/8/2/5 monoclonal 11/8/2/5 that was transfected with a short hairpin RNA sequence targeting SLC39A4, EV empty vector, Ov-SLC39A4-4/43/9/48 monoclonal 4/43/9/48 that was transfected with a SLC39A4 overexpression plasmid. The data is presented as the mean value ± standard deviation, and p < 0.05 was considered statistically significant.

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