间歇性缺氧
缺氧(环境)
内皮素1
伤口愈合
癌症研究
细胞生长
血管内皮生长因子
化学
内分泌学
医学
内科学
阻塞性睡眠呼吸暂停
免疫学
血管内皮生长因子受体
受体
生物化学
有机化学
氧气
作者
Mélanie Minoves,Florence Hazane-Puch,Giorgia Moriondo,Antoine Boutin-Paradis,Emeline Lemarié,Jean-Louis Pépin,Diane Godin-Ribuot,Anne Briançon-Marjollet
摘要
Obstructive sleep apnea (OSA) is an emerging risk factor for cancer occurrence and progression, mainly mediated by intermittent hypoxia (IH). Systemic IH, a main landmark of OSA, and local sustained hypoxia (SH), a classical feature at the core of tumors, may act separately or synergistically on tumor cells. Our aim was to compare the respective consequences of intermittent and sustained hypoxia on HIF-1, endothelin-1 and VEGF expression and on cell proliferation and migration in HepG2 liver tumor cells. Wound healing, spheroid expansion, proliferation and migration were evaluated in HepG2 cells following IH or SH exposure. The HIF-1α, endothelin-1 and VEGF protein levels and/or mRNA expression were assessed, as were the effects of HIF-1 (acriflavine), endothelin-1 (macitentan) and VEGF (pazopanib) inhibition. Both SH and IH stimulated wound healing, spheroid expansion and proliferation of HepG2 cells. HIF-1 and VEGF, but not endothelin-1, expression increased with IH exposure but not with SH exposure. Acriflavine prevented the effects of both IH and SH, and pazopanib blocked those of IH but not those of SH. Macitentan had no impact. Thus, IH and SH stimulate hepatic cancer cell proliferation via distinct signaling pathways that may act synergistically in OSA patients with cancer, leading to enhanced tumor progression.
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