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Fig. 7 | Journal of Hematology & Oncology

Fig. 7

From: Metformin potentiates the effect of arsenic trioxide suppressing intrahepatic cholangiocarcinoma: roles of p38 MAPK, ERK3, and mTORC1

Fig. 7

The role of AMPK, p38 MAPK, and ERK3 in metformin and ATO-induced mTORC1 inhibition in ICC cells. a The expression level of p-p38 MAPK/p38 MAPK and ERK3 was detected by western blot in ICC cells that were treated with metformin and ATO and in which AMPK or p-p38 MAPK was inhibited by siRNA or inhibitors (* P < 0.05). b The activation status of AMPK, p38 MAPK, ERK3, and mTORC1 was detected by western blot in ICC cells treated with AICAR and ATO. (Combination vs AICAR * P < 0.05, combination vs ATO # P < 0.05). c The activation status of mTORC1 was detected by western blot in ICC cells that were treated with metformin and ATO and in which AMPK or p-p38 MAPK was inhibited by siRNA or inhibitors (* P < 0.05). d The activation status of mTORC1 was detected by western blot in ICC cells treated with metformin and ATO and MAPK6-specific siRNA to downregulate ERK3 (* P < 0.05). e The proposed relationship between AMPK, p38 MAPK, and ERK3 in response to metformin- and ATO-induced mTORC1 inhibition in ICC cells. The green lines indicate the inhibition of mTORC1 by metformin and ATO. The red lines indicate the activation of mTORC1 by ATO

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