Table 1.
Potential therapeutic targets of CAAs in ovarian cancer
| Strategy | Targets and drugs | Preclinical and clinical effects | Reference |
|---|---|---|---|
| Targeting lipid supply | Inhibitor of CD36 | Reduce FA uptake by tumor cells and inhibit adipocyte-mediated proliferation and invasion | [96] |
| FASN inhibition | Reduce FA generation and the energy utilization of tumor cells | [122] | |
| MCT1 inhibition | Reduce tumor growth and increase intra-tumor lactate | [111] | |
| Autophagy inhibition | Reduce FA release and attenuate the ability of tumor cells to utilize FAs | [123] | |
| Targeting CAAs-derived soluble factors | Monoclonal antibody against VEGF-A | Inhibit the proliferation, angiogenesis and metastasis | [124] |
| Inhibitor of FABP4 | Reduce the ability of tumor cells to adapt to and colonize adipocyte--rich TME and promote the sensitivity to carboplatin | [79] | |
| Inhibitor of ANGPTL4 | Promote the sensitivity to chemotherapy | [80] | |
| Inhibitor of AA | Promote cisplatin-induced apoptosis of tumor cells | [81] | |
| Inhibitor of CCR5 (Maraviroc) | Reduce the recruitment and polarization of TAMs, thereby inhibit tumor cell growth and metastasis | [125] | |
| Thymoquinone | Reduce the pro-inflammatory factors produced by CAAs such as IL-6 and IL-1β, thereby prevente the progression of tumor cells | [126] | |
| Targeting lipid-derived EVs | miR-21 | Inhibit the apoptosis and chemoresistance of ovarian cancer cell | [83] |
| miR-181 | Increase the sensitivity to chemotherapy | [84] | |
| miR-424 | Reduce the proliferation and angiogenesis of tumor cells | [86] | |
| Targeting lipid metabolism | PPAR-γ inhibiton (GW9662) | Promote tumor cell apoptosis and improve the effect of chemotherapy | [115] |
| Aspirin | Alter the metabolomic and FA composition of adipocytes and inhibit tumor cell growth and metastasis | [127] | |
| Targeting the formation of CAAs | Metformin | Inhibit the differentiation of ADSCs into adipocytes, thereby inhibit the proliferation and invasion of tumor cells | [128] |
| Epigallocatechin-3-gallate (EGCG) | Inhibit the differentiation of ADSC into adipocytes, thereby prevent the invasive phenotype of tumor cells | [129] |
FASN, fatty acid synthase; MCT1, monocarboxylate transporter 1; VEGF-A, vascular endothelial growth factor A; FABP4, fatty acid binding protein 4; ANGPTL4, angiopoietin like protein 4; AA, arachidonic acid; CCR5, chemokine C-C-motif receptor 5; PPAR-γ, peroxisome proliferator-activated receptor-γ; FAs, fatty acids; EVs, extracellular vesicles; ADSCs, adipose-derived stem/stromal cells.