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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

From: Aberrant fatty acid profile and FFAR4 signaling confer endocrine resistance in breast cancer

Fig. 6

FFAR4-induced tamoxifen resistance is dependent on ERK and AKT pathways. a MCF-7 cells were transfected with scramble shRNA (Scr) or FFAR4 shRNA (FFAR4 KD) expressing constructs. b Cell viability of MCF-7 Scr/FFAR4 KD cells treated with 4OHT (8 μM) combined with DHA (50 μM), TUG891 (10 μM) or vehicle. c MCF-7 cells were seeded in 6-well plates for 48 h then treated with DHA (100 μM) or TUG891 (10 μM); d MCF-7 cells were seeded in 6-well plates for 48 h then treated with TUG891 (10 μM) combined with vehicle or AH7614 (10 μM); e MCF-7 Scr or FFAR4 KD cells were seeded in 6-well plates for 48 h then treated with TUG891 (10 μM); c-e cells were seeded in 6-well plates for 48 h then treated for the indicated time; phospho-ERK, ERK, phospho-AKT, AKT were measured by immunoblotting, the numbers above the lanes indicate the ratio of pERK/ERK and pAKT/AKT. GAPDH was used as loading control. f and g MCF-7 cells were seeded in 96-well plates for 48 h, then treated with 4OHT (8 μM) combined with DHA (50 μM), TUG891 (10 μM) or vehicle for 48 h, ERK1/2 inhibitor SCH772984 (10 μM) (f) or AKT inhibitor MK2206 (5 μM) (g) were added 30 min prior to other reagents, cell viabilities were measured using WST-1 substrates. The results shown are representative of three independent experiments. 4OHT, 4-hydroxytamoxifen. Error bars represent standard deviation. n.s.: not significant, *** P <  0.001

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