Fig. 4: MSCs activate AMPK pathway to enhance mitochondrial function of cancer cells. | Cell Death & Disease

Fig. 4: MSCs activate AMPK pathway to enhance mitochondrial function of cancer cells.

From: Mesenchymal stem cells in tumor microenvironment: drivers of bladder cancer progression through mitochondrial dynamics and energy production

Fig. 4

GO (a) and KEGG pathway (b) enrichment analyses of the 73 differential expression proteins. Immunoblot showed that expression of PKA, LKB1 on UMUC-3 was significantly up-regulated and then phosphorylate AMPK after coculture with MSCs for 12 h and 24 h (c). AMPKi dorsomorphin effectively inhibited the AMPK pathway, thereby attenuating the activating effect of MSCs on AMPK (d). The promotion of MSCs to the expression of BC cells of PGC1α, NRF1, TFAM, DRP1, and MFN2 no longer exists in the presence of AMPKi (e). Improved mitochondrial morphology and increased mitochondrial numbers of BC caused by MSCs were disrupted by AMPKi (f). MMP hyperpolarization of UMUC-3 induced by MSCs could be disrupted by AMPKi (g). Colony formation assays (h) and wound closure assays(i) showed that AMPKi administration could decrease the proliferation and migration of BC and disrupt the pro-tumor effect of MSCs on BC. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

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