Table 3 Roles and mechanisms of FAO in endocrinotherapy resistance.
From: The role and mechanism of fatty acid oxidation in cancer drug resistance
Cancer | Drug | Mechanism | Role | Ref |
|---|---|---|---|---|
BC | Tamoxifen | Low expression of GPR81 disrupts the Rap1 pathway, leading to up-regulation of PPARα and CPT1, thereby enhancing FAO | PR | [24] |
BC | Tamoxifen | Transcription factor c-Jun is activated by phosphorylation mediated by JNK kinase, which in turn activates CPT1A leading to FAO enhancement | PR | [144] |
BC | Endoxifen | The interaction between AMPK and AKT enhances FAO through the ERRα/PGC-1β/MCAD axis | PR | [146] |
BC | Tamoxifen/Fulvestrant | FAO enhancement leads to activation of Src pathway, which leads to drug resistance in cancer cells | PR | [147] |
BC | Fluvestine | FDXR enhances FAO by up-regulating CPT1A | PR | [149] |
PCa | 2-hydroxiflutamide | The down-regulated expression of PGC1α resulted in the inhibition of FAO | PR | [153] |
PCa | Enzalutamide | – | PR | [154] |
PCa | Enzalutamide | Increased expression of DECR2 led to increased FAO | PR | [155] |
PCa | AUY922 | – | PR | [51] |
