RESUMEN
In tumors, the rapid proliferation of cells and the imperfect blood supply system lead to hypoxia, which can regulate the adaptation of tumor cells to the hypoxic environment through hypoxia-inducible factor-1α (HIF-1α) and promote tumor development in multiple ways. Recent studies have found that epithelial-mesenchymal transition (EMT) and ferroptosis play important roles in the progression of tumor cells. The activation of HIF-1α is considered a key factor in inducing EMT in tumor cells. When HIF-1α is activated, it can regulate EMT-related genes, causing tumor cells to gradually lose their epithelial characteristics and acquire more invasive mesenchymal traits. The occurrence of EMT allows tumor cells to better adapt to changes in the surrounding tissue, enhancing their migratory and invasive capabilities, thus promoting tumor progression. At the same time, HIF-1α also plays a crucial regulatory role in ferroptosis in tumor cells. In a hypoxic environment, HIF-1α may affect processes such as iron metabolism and oxidative stress responses, inducing ferroptosis in tumor cells. This article briefly reviews the dual role of HIF-1α in EMT and ferroptosis in tumor cells, helping to gain a deeper understanding of the regulatory pathways of HIF-1α in the development of tumor cells, providing a new perspective for understanding the pathogenesis of tumors. The regulation of HIF-1α may become an important strategy for future tumor therapy.
Asunto(s)
Transición Epitelial-Mesenquimal , Ferroptosis , Subunidad alfa del Factor 1 Inducible por Hipoxia , Neoplasias , Humanos , Subunidad alfa del Factor 1 Inducible por Hipoxia/metabolismo , Neoplasias/metabolismo , Neoplasias/patología , AnimalesRESUMEN
Glioblastoma is the most aggressive and common intracranial malignant tumor, and the prognosis is still poor after various treatments. Based on the poor prognosis of glioma, new drugs that suppress the rapid progression and aggressive growth of glioma are urgently needed. It has been reported that nitidine chloride (NC) can inhibit tumor growth and epithelial-mesenchymal transition (EMT), and EMT is associated with cancer stem cell properties. The present study aimed to investigate the inhibitory effect of NC on the EMT process and stem cell-like properties in glioma cells. The results showed that the migration and invasion abilities in U87 and LN18 glioma cells were significantly increased after the induction of EMT and these effects were inhibited by NC in a concentration-dependent manner. NC treatment decreased the expression of EMT markers in glioma cells and self-renewal capacity of glioma stem-like cells. We demonstrated that these effects of NC were achieved via JAK2/STAT3 signaling. Taken together, these results indicate that NC inhibits the EMT process and glioma stem-like properties via JAK2/STAT3 signaling pathway, suggesting that NC may be a potential anti-glioma drug.