Hyperbaric oxygen promotes not only glioblastoma proliferation but also chemosensitization by inhibiting HIF1α/HIF2α-Sox2.
Hyperbaric oxygen promotes not only glioblastoma proliferation but also chemosensitization by inhibiting HIF1α/HIF2α-Sox2.
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高压氧不仅促进胶质母细胞瘤增殖,还通过抑制 HIF1α/HIF2α-Sox2 促进化疗增敏
DOI:
10.1038/s41420-021-00486-0
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发表时间:
2021-05-13
影响因子:
7
通讯作者:
Liao B
中科院分区:
文献类型:
--
作者:
Wang P;Gong S;Pan J;Wang J;Zou D;Xiong S;Zhao L;Yan Q;Deng Y;Wu N;Liao B
There exists a consensus that combining hyperbaric oxygen (HBO) and chemotherapy promotes chemotherapy sensitivity in GBM cells. However, few studies have explored the mechanism involved. HIF1α and HIF2α are the two main molecules that contribute to GBM malignant progression by inhibiting apoptosis or maintaining stemness under hypoxic conditions. Moreover, Sox2, a marker of stemness, also contributes to GBM malignant progression through stemness maintenance or cell cycle arrest. Briefly, HIF1α, HIF2α and Sox2 are highly expressed under hypoxia and contribute to GBM growth and chemoresistance. However, after exposure to HBO for GBM, whether the expression of the above factors is decreased, resulting in chemosensitization, remains unknown. Therefore, we performed a series of studies and determined that the expression of HIF1α, HIF2α and Sox2 was decreased after HBO and that HBO promoted GBM cell proliferation through cell cycle progression, albeit with a decrease in stemness, thus contributing to chemosensitization via the inhibition of HIF1α/HIF2α-Sox2.
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影响因子:
7
作者:
Wang P;Wan WW;Xiong SL;Feng H;Wu N
通讯作者:
Wu N
DOI:
10.1007/s12032-016-0814-0
发表时间:
2016-09
期刊:
Medical oncology (Northwood, London, England)
影响因子:
--
作者:
Stępień K;Ostrowski RP;Matyja E
通讯作者:
Matyja E
DOI:
10.1007/s13402-018-0374-8
发表时间:
2018-06
期刊:
Cellular oncology (Dordrecht, Netherlands)
影响因子:
--
作者:
Ahmed EM;Bandopadhyay G;Coyle B;Grabowska A
通讯作者:
Grabowska A
影响因子:
2.9
作者:
Wang, Yong-Gang;Zhan, Yi-Ping;Yu, Chun-Jiang
通讯作者:
Yu, Chun-Jiang
影响因子:
82.9
作者:
Young, Regina M.;Simon, M. Celeste
通讯作者:
Simon, M. Celeste