The Role of NF-κB/MIR155HG in Regulating the Stemness and Radioresistance in Breast Cancer Stem Cells.

BACKGROUND

Breast cancer stem cells (BCSCs) are instrumental in treatment resistance, recurrence, and metastasis. The development of breast cancer and radiation sensitivity is intimately pertinent to long non-coding RNA (lncRNA). This work is formulated to investigate how the lncRNA affects the stemness and radioresistance of BCSCs.

METHODS

Effects of knockdown on BCSCs were gauged in MCF-7 and MDA-MB-231 cell lines. expression was manipulated in cells, followed by an assessment of stemness, DNA damage repair, apoptosis, cell cycle, and the Wnt signaling pathway under radiation conditions. The interaction between nuclear factor kappa B (NF-κB) subunit RelA and was examined using a dual-luciferase reporter assay. To examine the binding interaction between RelA and promoter, chromatin immunoprecipitation was performed.

RESULTS

Breast cancer-derived stem cells exhibited a high level of . Knockdown of reduced stemness, enhanced radiosensitivity, induced apoptosis, and arrested cells in the G1 phase. Mechanistically, knockdown repressed Wnt/β-catenin signaling and mediated apoptosis-related protein expressions. NF-κB subunit RelA transcriptionally activated , thereby contributing to radioresistance in BCSCs.

CONCLUSION

NF-κB regulates transcriptionally to activate the Wnt pathway, thus enhancing stemness and radioresistance in BCSCs. Targeting may enhance the susceptibility of cancer stem cells to radiation-induced cell death, potentially improving therapeutic outcomes. These findings underscore as a promising therapeutic target for breast cancer.