Fig. 4: SIRT5 mediates the desuccinylation of MTHFD2 to maintain ROS homeostasis and delay cellular senescence. | Communications Biology

Fig. 4: SIRT5 mediates the desuccinylation of MTHFD2 to maintain ROS homeostasis and delay cellular senescence.

From: SIRT5-mediated desuccinylation of MTHFD2 enhances chemoresistance in breast cancer cells by reducing therapy-induced senescence

Fig. 4

A HFF cells (P30) that express FLAG-MTHFD2 and FLAG-MTHFD2 K44E were transfected with siMTHFD2, the ROS level was determined by flow cytometry analysis. B Effect of ectopic expression of WT MTHFD2 and MTHFD2 K44E mutant on cellular senescence. HFF cells (P30) were transfected with siMTHFD2 or siControl to knock down the endogenous MTHFD2, and then express FLAG-MTHFD2 and FLAG-MTHFD2 K44E. The cellular senescence was indicated by SA-β-gal staining. C HFF cells (P30) that were transfected with siMTHFD2 to knock down the endogenous MTHFD2, and express FLAG-MTHFD2 K44E, and add or not add the 2 mM ROS scavenger(NAC), the ROS level was determined by immunofluorescence. D Senescence-associated β-galactosidase activity was assessed in serially passaged HFF cells (P50) following treatment with NAC (2 mM). E HFF cells (P18) transfected with SIRT5 siRNA or control siRNA, the relative ROS level was determined by flow cytometry analysis. F Effect of SIRT5 silencing (siSIRT5) and siControl on HFF (P18) cellular senescence. G HFF (P18) were cultured in medium and then transfected with siSIRT5 and siControl, respectively. The cellular senescence was indicated by SA-β-gal staining. H HFF cells (P30) were transfected with siRNA to knock down the endogenous SIRT5, and then expressed FLAG-MTHFD2 and FLAG-MTHFD2 K44E. The cellular senescence was indicated by SA-β-gal staining.

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