Fig. 4: Effect of 20(S)-Rh2E2 on the metabolic reprograming of LLC-1 cancer cells. | Cell Death & Disease

Fig. 4: Effect of 20(S)-Rh2E2 on the metabolic reprograming of LLC-1 cancer cells.

From: Novel ginsenoside derivative 20(S)-Rh2E2 suppresses tumor growth and metastasis in vivo and in vitro via intervention of cancer cell energy metabolism

Fig. 4

a The comparison of glycolytic profile of LLC-1 cells upon the treatment of 20(S)- or 20(R)-Rh2E2. The glycolytic function was measured by directly detecting the ECAR of cells. The compounds (glucose, oligomycin, 2-DG) were serially injected to measure the glycolysis and glycolytic capacity, respectively. b The comparison of mitochondrial respiration profile of LLC-1 cells upon the treatment of 20(S)- or 20(R)-Rh2E2. Mitochondrial respiration test determines the key parameters of mitochondrial function by directly measuring the OCR of cells. The compounds (oligomycin, FCCP, and a mix of rotenone and antimycin A) were serially injected to measure the basal respiration, ATP production, and maximal respiration, respectively. c The comparison of glycolytic profile of CCD19Lu cells upon the treatment of 20(S)- or 20(R)-Rh2E2. d The comparison of mitochondrial respiration profile of LLC-1 cells upon the treatment of 20(S)- or 20(R)-Rh2E2. e 20(S)-Rh2E2 and 20(R)-Rh2E2 decreased the ATP production in LLC-1 cancer cells. f 20(S)-Rh2E2 and 20(R)-Rh2E2 enhanced the ATP generation in CCD19Lu normal cells. The amount of energy metabolites was calculated as pmol/106 cells. g 20(S)-Rh2E2 and 20(R)-Rh2E2 specifically reduced the production of acetyl CoA in LLC-1 lung cancer cells, but not CCD19Lu normal cells. h 20(S)-Rh2E2 and 20(R)-Rh2E2 enhanced the accumulation of α-ketoglutarate, the energy metabolite of TCA cycle in LLC-1 cells.

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