Table 4. Effects and potential mechanisms of eustress on cancer treatment in EE models.
↑, increase; ↓, decrease; →, causal; NR, not report; ATP, adenosine triphosphate; CCR5, C-C chemokine receptor 5; M2-TAM, M2 tumor–associated macrophages.
| Cancer type | Effects on tumor | Effects on TME | Mechanism | Reference |
| Melanoma, colon cancer | ↓ Tumorigenesis, growth | ↓VEGF ↑NK cell, CD8+ function |
↑Hypothalamic-derived BDFN → ↑β-AR → ↓leptin ↑lipocalin production in adipose tissue |
(85) |
| Intracranial glioma | ↓Tumor growth | ↑IL-15, BDFN ↓NK cell, microglia/macrophage |
↑Brain IL-15 → ↑NK cell ↑brain BDFN → ↓microglia/macrophage infiltration and activation |
(86) |
| Mammary cancer | ↓Tumor growth | NR | Cross-talk between changed signaling pathways and adipokine/cytokine secretions in muscle, adipose tissue, and tumor |
(95) |
| Mammary cancer | ↓Tumor growth | COX-2 expression | ↓Intratumoral COX-2 → inflammatory state ↓plasma ratio of adiponectin and leptin |
(96) |
| Pancreatic cancer | ↓Tumor growth | NR | ↓Mitochondria-related genes (encoding key enzymes of the citrate cycle and pyruvate decarboxylation) in cancer cells |
(97) |
| Pancreatic cancer, lung cancer | ↓Tumor growth | ↑ NK cell | β-AR↑ → ↑expression of CCR5 and NKG2D on NK cell → NK cell function |
(20) |
| Hepatocellular carcinoma | ↓ Tumorigenesis, growth ↑response to anti–PD-1 mAb |
↓Immune suppression (↑CD8+ T; ↓MDSC, M2-TAM) |
SNS → β-AR → ↓CCL2/CCR2 → ↓chemotaxis of MDSC and M2-TAM |
(19) |
| Pancreatic cancer | ↑Response to chemotherapy | NR | ↓Tumoral ATP-binding cassette transporter A8b |
(101) |