2023年5月1日 · Effects of FOXM1 expression status on ROS regulation in OSCC cell lines. Representative images and quantitative analysis of the immunofluorescence of ROS/SOD under FOXM1 knockdown or overexpressing conditions after exposure to 6-Gy X-ray IR.

CSCs with increased OXPHOS levels maintained low ROS levels by coupling FoxM1-dependent Prx3 expression and fatty acid oxidation-mediated NADPH regeneration. Thus, interventions targeting ROS homeostasis in CSCs may be a useful strategy for targeting this drug-resistant tumor cell subpopulation.

Western blot analysis showed that increased ROS levels can activate FOXM1 expression and that inhibiting ROS generation significantly reduced the expression of FOXM1. These findings provide new insight and evidence that the NOX4/ROS pathway is involved in the upregulation of FOXM1 expression in glioblastoma cells.

2009年8月20日 · We show that induction of FoxM1 by oncogenic Ras requires ROS. Elevated FoxM1, in turn, downregulates ROS levels by stimulating expression of ROS scavenger genes, such as MnSOD, catalase and PRDX3. FoxM1 depletion sensitizes cells to oxidative stress and increases oncogene‐induced premature senescence.

2023年8月24日 · Few studies have reported the relationship between ferroptosis and FOXM1, and our study revealed that FOXM1 inhibits ferroptosis by increasing FA synthesis, reducing the accumulation of ROS...

2024年11月1日 · To investigate the effects of FOXM1 on oxidative stress and mitochondrial function during oocyte aging, we assessed the levels of ROS, GSH, CAT, SOD, T-AOC, and ATP after inhibition of FOXM1. Compared with MII oocytes, aging oocytes exhibited significantly increased ROS levels and significantly decreased levels of GSH, CAT, SOD, T-AOC, and ATP ...

2022年2月1日 · FOXM1 increased lipid droplet to protect cells from paclitaxel induced ROS. Inhibitor of PLD1 sensitizes metastatic cancer cells to paclitaxel therapy. Chemoresistance is a major challenge for the treatment of cancer with metastasis. We investigated the mechanisms of lipid metabolites involved in drug resistance.

我们表明致癌 Ras 对 FoxM1 的诱导需要 ROS。反过来，升高的 FoxM1 通过刺激 ROS 清除基因（如 MnSOD、过氧化氢酶和 PRDX3）的表达来下调 ROS 水平。FoxM1 耗竭使细胞对氧化应激敏感并增加致癌基因诱导的过早衰老。

CSCs with increased OXPHOS levels maintained low ROS levels by coupling FoxM1-dependent Prx3 expression and fatty acid oxidation-mediated NADPH regeneration. Thus, interventions targeting ROS homeostasis in CSCs may be a useful strategy for targeting this drug-resistant tumor cell subpopulation.

In this study, we show that expression of FoxM1 is induced by increased oncogenic stress requiring ROS, and that the upregulated FoxM1 in a negative feedback loop counteracts elevated intracellular ROS levels by stimulating the expression of anti-oxidant enzyme genes to protect dividing cells and tumour cells from oxidative stress.