Correlation between p65 and TNF-α in patients with acute myelocytic leukemia

Abstract

Abstract. The correlation between the expression levels of p65 and TNF-α in patients with acute myelocytic leukemia (AML) and AML cell lines were investigated. The bone marrow samples of 30 AML patients and 10 non-leukemia controls were studied. The mRNA expression levels of p65 and TNF-α were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and Pearson's Correlation test was used to demonstrate the correlation between TNF-α and p65 expression levels in AML specimens. Receiver operating characteristic (ROC) curves were plotted to determine whether TNF-α and p65 expression levels could be used to differentiate AML samples from non-leukemia samples. MG132 and anti-TNF-α antibody were used to inhibit the expression of p65 and TNF-α in the AML cell line, HL-60. The expression of p65 and TNF-α were detected by RT-qPCR and western blot analysis. The mRNA expression levels of p65 and TNF-α were significantly increased in AML patients compared with non-leukemia control bone marrow samples by RT-qPCR, and the two molecules expression pattern's exhibited sufficient predictive power to distinguish AML patients from non-leukemia control samples. Pearson's correlation analysis demonstrated that TNF-α expression was strongly correlated with p65 expression in AML bone marrow samples. In HL-60 cells, inhibition of TNF-α reduced the expression of p65; in addition, inhibition of p65 reduced the expression of TNF-α as assessed by RT-qPCR and western blot analysis. p65 and TNF-α were highly expressed in AML patients, and these 2 molecules were strongly correlated. The present study indicates that p65 and TNF-α have potential as molecular markers to distinguish AML patients from non-leukemia control samples, and that these 2 molecules may be useful prognostic factor for patients with AML.

Exploring the mechanism of fraxetin against acute myeloid leukemia through cell experiments and network pharmacology

“…Zhou et al found that curcumin can inhibit the phosphorylation of AKT in AML cells, thereby inducing apoptosis and inhibiting cell proliferation [ 23 ]. TNFs, including TNF-α and TNF-β, are central regulators of inflammation and have been linked to the occurrence and progression of many types of cancer, including AML; furthermore, TNFs can promote the production of leukemia stem cells [ 24 ]. In addition, upregulation of TNF-α expression can induce the accumulation of reactive oxygen species (ROS), leading to the apoptosis of AML stem cells [ 25 ].…”

Identification and validation of signal recognition particle 14 as a prognostic biomarker predicting overall survival in patients with acute myeloid leukemia

“…Regarding the MAPK signaling pathway in AML, mesenchymal stromal cells can regulate the apoptosis repressor with caspase recruitment domain in AML by activating MAPK and PI3K signaling pathways, thereby affecting drug resistance and prognosis, and can thus be used as a potential therapeutic target for AML [ 19 ]. Dong et al suggested that TNF-α expression was significantly increased in AML patients, and ROC curve analysis indicated that it could be used to differentiate between AML and nonleukemia samples [ 20 ]. TCR is widely used in the treatment of hematologic malignancies.…”

Identification and validation of signal recognition particle 14 as a prognostic biomarker predicting overall survival in patients with acute myeloid leukemia

“…Regarding the MAPK signaling pathway in AML, mesenchymal stromal cells can regulate the apoptosis repressor with caspase recruitment domain in AML by activating MAPK and PI3K signaling pathways, thereby affecting drug resistance and prognosis, and can thus be used as a potential therapeutic target for AML [19]. Dong et al suggested that TNF-α expression was signi cantly increased in AML patients, and ROC curve analysis indicated that it could be used to differentiate between AML and nonleukemia samples [20]. TCR is widely used in the treatment of hematologic malignancies.…”