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Fig. 7 | Journal of Biomedical Science

Fig. 7

From: Reprogramming of arachidonate metabolism confers temozolomide resistance to glioblastoma through enhancing mitochondrial activity in fatty acid oxidation

Fig. 7

Schematic representation of the working model. According to established gene expression profiles and ω-3/6 fatty acid metabolome, we found that Sp1 increased the PTGS2 expression and PGE2 production in recurrent GBM patients and in TMZ-resistant GBM cells. For inducing TMZ resistance, PGE2 activated mitochondrial FAO and TCA cycle progression through enhancing mitochondrial fusion. These results showing the role of PGE2 metabolism in GBM provide us a new strategy to attenuate drug resistance or to re-sensitize recurred glioblastoma

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Journal of Biomedical Science

ISSN: 1423-0127