The potential roles of HIF-1α in epithelial-mesenchymal transition and ferroptosis in tumor cells.

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.

Nitidine chloride suppresses epithelial-mesenchymal transition and stem cell-like properties in glioblastoma by regulating JAK2/STAT3 signaling.

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.