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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: CHTM1 regulates cancer cell sensitivity to metabolic stress via p38-AIF1 pathway

Fig. 5

CHTM1 modulates p38 phosphorylation under metabolic stress condition. (a) Western blot analyses showing increased p38 phosphorylation in CHTM1 knockdown A549 cells following 4-h glucose/glutamine starvation (b) Western blot analyses showing p38 inhibitor SB203580 (p38i) abrogates Hsp27 phosphorylation in CHTM1 knockdown A549 cells (lanes 7–9). Cells were pretreated with the inhibitor (10 μM) for 2 h and then starved for glucose/glutamine for 4 h. (c) Western blot analyses showing increased p38 phosphorylation in CHTM1 knockdown A549 and H1299 lung cancer cells following 50 mM metformin treatment for 12 h. (d) Western blot analyses showing decrease in p38 phosphorylation in CHTM1 overexpressing A549 cells starved for glucose/glutamine for 4 h. (e) Western blot analyses showing p38 inhibitor SB203580 (p38i) abrogates MAPKAP2 phosphorylation in CHTM1 overexpressing A549 cells (compare lanes 3&4). Cells were pretreated with the inhibitor (10 μM) for 2 h and then starved for glucose/glutamine for 4 h. (f) Western blot analyses showing decreased p38 phosphorylation in CHTM1 overexpressing A549 cells following 50 mM metformin treatment for 12 h. (g) CHTM1 overexpression regulates p38 activity under metabolic stress. A549 cells were co-transfected with CHTM1 or empty vector and ATF2 promoter luciferase construct for 48 h and luciferase assay was performed 4-h after glucose/glutamine deprivation or 12-h after 50 mM metformin

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