fig2

Fra-1 affects chemotherapy sensitivity by inhibiting ferroptosis in gastric cancer cells

Figure 2. Fra-1 activates the PPP pathway in GC cells. (A) Heatmap showing the relative abundance of non-targeted metabolites in the NC group versus the Fra-1 overexpression group in GC cells (n = 6); (B) Expression levels of PPP metabolites; (C-F) RT-qPCR analysis of key molecules in the PPP metabolism pathway after overexpression/knockdown of Fra-1 in GC cells AGS and HGC27; (G and H) Protein levels of key molecules in the metabolic pathway of the PPP after overexpression/knockdown of Fra-1 in GC cells AGS and HGC27 detected by western blot assay; (I and J) G6PD enzyme activity measured after overexpression/knockdown of Fra-1 in GC cells AGS and HGC27 using the G6PD enzyme activity kit; (K and L) NADPH content measured after overexpression/knockdown of Fra-1 in GC cells AGS and HGC27 using the NADPH kit; (M and N) ROS content measured after overexpression/knockdown of Fra-1 in GC cells AGS and HGC27 using the ROS kit. All experiments were performed with three technical replicates. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. Fra-1: Fos-related antigen-1; PPP: pentose phosphate pathway; GC: gastric cancer; G6PD: glucose-6-phosphate dehydrogenase; NADPH: nicotinamide adenine dinucleotide phosphate; ROS: reactive oxygen species.

Cancer Drug Resistance
ISSN 2578-532X (Online)

Portico

All published articles will preserved here permanently:

https://www.portico.org/publishers/oae/

Portico

All published articles will preserved here permanently:

https://www.portico.org/publishers/oae/