Purpose: Studies have shown that intermittent hypoxia (IH) alters host immune functions and promotes tumor growth. However, the relevant mechanisms of these effects have not been completely elucidated. We hypothesized that IH promotes the growth of tumors by changing cytokine levels in the tumor microenvironment and inducing immune escape.
Methods: Sarcoma-180 (S180) solid tumor cells were injected into the right flank of Kunming mice. The mice were then randomly divided into the IH and room air (RA) groups. The mice were euthanized 2 weeks after IH exposure, and the weight of tumor tissues was measured. Next, IL-6, IL-17, IL-10, and TNF-α levels in tumor tissues were measured via enzyme linked immunosorbent assay (ELISA), and hypoxia inducible factor-1α (HIF-1α) and transforming growth factor β (TGF-β) expressions were examined through Western blot analysis.
Results: Two weeks of IH exposure significantly accelerated the growth of S180 solid tumors. Western blot analysis results showed that the expression levels of HIF-1α and TGF-β in S180 tumors in the IH group were significantly upregulated compared with those in the RA group. ELISA results showed that compared with the RA group, the IH group had significantly increased TNF-α and IL-10 (P < 0.05) and significantly decreased IL-17 (P < 0.05).
Conclusion: IH might promote the growth of S180 solid tumors by inhibiting the antitumor immune response and inducing tumor immune escape via the upregulation of TGF-β.
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