缺氧诱导因子-1α通过激活细胞焦亡信号轴促进胶质瘤的增殖和侵袭。
HIF-1α facilitates glioma proliferation and invasion by activating pyroptosis signaling axis.
作者信息
Wang Xin-Wei, Fu Hao, Zhang Ya-Min
机构信息
The First Central Clinical School, Tianjin Medical University, Tianjin, 300142, China.
Department of General Medicine, Characteristic Medical Center of PAP, Tianjin, 300162, China.
出版信息
Chin Neurosurg J. 2024 May 11;10(1):14. doi: 10.1186/s41016-024-00366-3.
BACKGROUND
HIF-1α is thought to be a novel regulator which contributes to carcinogenesis. However, the mechanism underlying the effect of HIF-1α in gliomas remains largely unknown.
METHODS
In the research, we demonstrate that HIF-lα mRNA and protein levels are elevated in glioma cells. The colony formation assays, transwell assays, and wound-healing assays showed that overexpression of HIF-1α promoted proliferation and invasion of glioma cells.
RESULTS
Overexpression of HIF-lα also increased the expression of inflammatory factors related to pyrolysis (TNF-α, IL-10, and IL-1β) and protein related to pyrolysis signal pathway (NLRP3, ASC, caspase-1, GSDMD, and GSDME).
CONCLUSIONS
Therefore, we speculate that HIF-1α promotes the proliferation and invasion of glial cells by regulating pyrolysis pathway. These results might provide a novel strategy and target for treatment of glioma.
背景
缺氧诱导因子-1α（HIF-1α）被认为是一种参与肿瘤发生的新型调节因子。然而，HIF-1α在胶质瘤中发挥作用的潜在机制仍 largely未知。
方法
在本研究中，我们证明胶质瘤细胞中HIF-1α的mRNA和蛋白质水平升高。集落形成试验、Transwell试验和伤口愈合试验表明，HIF-1α的过表达促进了胶质瘤细胞的增殖和侵袭。
结果
HIF-1α的过表达还增加了与焦亡相关的炎症因子（肿瘤坏死因子-α、白细胞介素-10和白细胞介素-1β）以及与焦亡信号通路相关的蛋白质（NLRP3、ASC、半胱天冬酶-1、Gasdermin D和Gasdermin E）的表达。
结论
因此，我们推测HIF-1α通过调节焦亡途径促进胶质细胞的增殖和侵袭。这些结果可能为胶质瘤的治疗提供一种新的策略和靶点。
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