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 lnc...

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Main Authors: Yunbao Xu, Lu Yang, Guangming Li, Chuangzhou Rao
Format: Article
Language:English
Published: IMR Press 2025-01-01
Series:Frontiers in Bioscience-Landmark
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Online Access:https://www.imrpress.com/journal/FBL/30/1/10.31083/FBL25810
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author Yunbao Xu
Lu Yang
Guangming Li
Chuangzhou Rao
author_facet Yunbao Xu
Lu Yang
Guangming Li
Chuangzhou Rao
author_sort Yunbao Xu
collection DOAJ
description 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 MIR155HG affects the stemness and radioresistance of BCSCs. Methods: Effects of MIR155HG knockdown on BCSCs were gauged in MCF-7 and MDA-MB-231 cell lines. MIR155HG 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 MIR155HG was examined using a dual-luciferase reporter assay. To examine the binding interaction between RelA and MIR155HG promoter, chromatin immunoprecipitation was performed. Results: Breast cancer-derived stem cells exhibited a high level of MIR155HG. Knockdown of MIR155HG reduced stemness, enhanced radiosensitivity, induced apoptosis, and arrested cells in the G1 phase. Mechanistically, MIR155HG knockdown repressed Wnt/β-catenin signaling and mediated apoptosis-related protein expressions. NF-κB subunit RelA transcriptionally activated MIR155HG, thereby contributing to radioresistance in BCSCs. Conclusion: NF-κB regulates MIR155HG transcriptionally to activate the Wnt pathway, thus enhancing stemness and radioresistance in BCSCs. Targeting MIR155HG may enhance the susceptibility of cancer stem cells to radiation-induced cell death, potentially improving therapeutic outcomes. These findings underscore MIR155HG as a promising therapeutic target for breast cancer.
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spelling doaj-art-c441c12dc9a04b708448593874bceae82025-01-25T08:55:52ZengIMR PressFrontiers in Bioscience-Landmark2768-67012025-01-013012581010.31083/FBL25810S2768-6701(24)01551-XThe Role of NF-κB/MIR155HG in Regulating the Stemness and Radioresistance in Breast Cancer Stem CellsYunbao Xu0Lu Yang1Guangming Li2Chuangzhou Rao3Department of Chemoradiotherapy, Ningbo No 2 Hospital, 315000 Ningbo, Zhejiang, ChinaDepartment of Chemoradiotherapy, Ningbo No 2 Hospital, 315000 Ningbo, Zhejiang, ChinaDepartment of Breast Surgery, Ningbo No 2 Hospital, 315000 Ningbo, Zhejiang, ChinaDepartment of Chemoradiotherapy, Ningbo No 2 Hospital, 315000 Ningbo, Zhejiang, ChinaBackground: 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 MIR155HG affects the stemness and radioresistance of BCSCs. Methods: Effects of MIR155HG knockdown on BCSCs were gauged in MCF-7 and MDA-MB-231 cell lines. MIR155HG 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 MIR155HG was examined using a dual-luciferase reporter assay. To examine the binding interaction between RelA and MIR155HG promoter, chromatin immunoprecipitation was performed. Results: Breast cancer-derived stem cells exhibited a high level of MIR155HG. Knockdown of MIR155HG reduced stemness, enhanced radiosensitivity, induced apoptosis, and arrested cells in the G1 phase. Mechanistically, MIR155HG knockdown repressed Wnt/β-catenin signaling and mediated apoptosis-related protein expressions. NF-κB subunit RelA transcriptionally activated MIR155HG, thereby contributing to radioresistance in BCSCs. Conclusion: NF-κB regulates MIR155HG transcriptionally to activate the Wnt pathway, thus enhancing stemness and radioresistance in BCSCs. Targeting MIR155HG may enhance the susceptibility of cancer stem cells to radiation-induced cell death, potentially improving therapeutic outcomes. These findings underscore MIR155HG as a promising therapeutic target for breast cancer.https://www.imrpress.com/journal/FBL/30/1/10.31083/FBL25810breast cancercancer stem cellsnuclear factor-kappa bmir155 host gene
spellingShingle Yunbao Xu
Lu Yang
Guangming Li
Chuangzhou Rao
The Role of NF-κB/MIR155HG in Regulating the Stemness and Radioresistance in Breast Cancer Stem Cells
Frontiers in Bioscience-Landmark
breast cancer
cancer stem cells
nuclear factor-kappa b
mir155 host gene
title The Role of NF-κB/MIR155HG in Regulating the Stemness and Radioresistance in Breast Cancer Stem Cells
title_full The Role of NF-κB/MIR155HG in Regulating the Stemness and Radioresistance in Breast Cancer Stem Cells
title_fullStr The Role of NF-κB/MIR155HG in Regulating the Stemness and Radioresistance in Breast Cancer Stem Cells
title_full_unstemmed The Role of NF-κB/MIR155HG in Regulating the Stemness and Radioresistance in Breast Cancer Stem Cells
title_short The Role of NF-κB/MIR155HG in Regulating the Stemness and Radioresistance in Breast Cancer Stem Cells
title_sort role of nf κb mir155hg in regulating the stemness and radioresistance in breast cancer stem cells
topic breast cancer
cancer stem cells
nuclear factor-kappa b
mir155 host gene
url https://www.imrpress.com/journal/FBL/30/1/10.31083/FBL25810
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