The mechanisms of tumor necrosis factor α in regulating Krüpple-like factor 4 expression in SK-BR-3 breast cancer cells

Caiyun Liu; Chengbao Feng; Haifei Li; Erying Zhang; Bo Liu; Ying Wang; Peng Wang

doi:10.1111/ajco.14046

The mechanisms of tumor necrosis factor α in regulating Krüpple-like factor 4 expression in SK-BR-3 breast cancer cells

Asia Pac J Clin Oncol. 2024 Jan 18. doi: 10.1111/ajco.14046. Online ahead of print.

Authors

Caiyun Liu¹, Chengbao Feng¹, Haifei Li¹, Erying Zhang¹, Bo Liu¹, Ying Wang¹, Peng Wang¹

Affiliation

¹ Department of Medical Oncology, The No. 2 Hospital of Baoding, Baoding, China.

PMID: 38235502
DOI: 10.1111/ajco.14046

Abstract

Objective: To explore the expression and functional role of Krüpple-like factor 4 (KLF4) protein stimulated by tumor necrosis factor α (TNF-α) in SK-BR-3 breast cancer cells.

Methods: SK-BR-3 cells were stimulated with various concentrations of TNF-α at 0, 1, 5, 10, and 20 ng/mL. Expression levels of KLF4 protein were detected by Western blotting. In the detection of apoptosis, flow cytometry, and DAPI staining were used for detecting the level of apoptosis.

Results: KLF4 expression was markedly elevated following stimulation of SK-BR-3 with TNF-α. At the same time, the expression of KLF4 protein increased gradually with the increase of TNF-α stimulation concentration. TNF-α stimulation of SK-BR-3 cells increased apoptosis as measured by apoptosis levels. By overexpressing KLF4 protein in SK-BR-3 cells, it similarly increased apoptosis and promoted cell death of SK-BR-3 cells.

Conclusion: TNF-α promotes KLF4 expression, while TNF-α promotes apoptosis in SK-BR-3 cells, a process that may be due to elevated KLF4 protein expression.

Keywords: KLF4; SK-BR-3 cells; TNF-α; apoptosis.