Fig. 3: AKR1C3 could enhance the radioresistance in EAC cells. | Cell Death & Disease

Fig. 3: AKR1C3 could enhance the radioresistance in EAC cells.

From: AKR1C3 enhances radioresistance in esophageal adenocarcinoma via inhibiting ferroptosis through suppressing TRIM21-mediated ubiquitination of HSPA5

Fig. 3: AKR1C3 could enhance the radioresistance in EAC cells.The alternative text for this image may have been generated using AI.

A Validation of AKR1C3 overexpression in OE33 and AKR1C3 knockdown in SKGT-4 was performed by western blot. B, C Survival fraction after 0–6 Gy irradiation in OE33 VEC/OE33 AKR1C3 and SKGT-4 shNT/SKGT-4 shAKR1C3. Cells were treated with irradiation: 3 Gy for OE33 (D) and 8 Gy for SKGT-4 (G). The fold change of the nuclear γ-H2AX foci was presented in the bar charts (E, F, H). I Validation of γ-H2AX protein levels in OE33P/R, OE33 VEC/AKR1C3, and SKGT-4 shNT/shAKR1C3 was performed by western blot. Cells were treated with irradiation: 3 Gy for OE33 and 8 Gy for SKGT-4. J, K Cells were treated with 0 or 10 Gy irradiation. Flow cytometry was performed 72 h after treatment. Bar charts showed the percentage of dead cells before or after irradiation in OE33 VEC/AKR1C3 and SKGT-4 shNT/shAKR1C3 by Annexin V and DAPI staining. Means ± SD, N = 3. Statistical comparisons were made using a paired two-tailed Student’s t-test; *P < 0.05, **P < 0.01, ***P < 0.001.

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