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BCL11B Predetermines a Persister State in Breast Cancer That Is Reversed by TNFα [Bulk RNA-seq]

ABSTRACT: Chemotherapy resistance remains a major obstacle to achieving cures in many cancer patients, yet the underlying causes for drug response diversity are poorly understood. Here, we systematically assessed the cellular differentiation status of human breast cancer cells utilizing single-cell atlases and identified a distinct population of immature basal-like cancer cells marked by BCL11B. Notably, higher levels of BCL11B+ cancer cells are significantly associated with early relapse in breast cancer patients who received chemotherapy. Using mouse and human breast cancer models, we found that BCL11B functions as a central regulator and delineates an immature cell state that preferentially transitions to a drug-resistant persister state during treatment through multiple pre-existing and adaptive drug-resistance programs. Importantly, the cytokine tumor necrosis factor alpha (TNFα) is revealed as a natural inhibitor of BCL11B and can directly reverse the emergence of chemoresistant persister cells. Therefore, we identify BCL11B as an unappreciated pre-determinant of drug response and a therapeutic target for a subset of breast cancer patients at high risk of developing chemoresistance.

ORGANISM(S): Mus musculus

PROVIDER: GSE228440 | GEO | 2026/08/31

REPOSITORIES: GEO

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BCL11B Predetermines a Persister State in Breast Cancer That Is Reversed by TNFα [scRNA-seq]

Project description:Chemotherapy resistance remains a major obstacle to achieving cures in many cancer patients, yet the underlying causes for drug response diversity are poorly understood. Here, we systematically assessed the cellular differentiation status of human breast cancer cells utilizing single-cell atlases and identified a distinct population of immature basal-like cancer cells marked by BCL11B. Notably, higher levels of BCL11B+ cancer cells are significantly associated with early relapse in breast cancer patients who received chemotherapy. Using mouse and human breast cancer models, we found that BCL11B functions as a central regulator and delineates an immature cell state that preferentially transitions to a drug-resistant persister state during treatment through multiple pre-existing and adaptive drug-resistance programs. Importantly, the cytokine tumor necrosis factor alpha (TNFα) is revealed as a natural inhibitor of BCL11B and can directly reverse the emergence of chemoresistant persister cells. Therefore, we identify BCL11B as an unappreciated pre-determinant of drug response and a therapeutic target for a subset of breast cancer patients at high risk of developing chemoresistance.

2026-08-31 | GSE228439 | GEO

BCL11B Predetermines a Persister State in Breast Cancer That Is Reversed by TNFα

Project description:BCL11B Predetermines a Persister State in Breast Cancer That Is Reversed by TNFα

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BCL11B Predetermines a Persister State in Breast Cancer That Is Reversed by TNFα [scRNA-seq]

Project description:BCL11B Predetermines a Persister State in Breast Cancer That Is Reversed by TNFα [scRNA-seq]

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Mkango2019 - Dynamics of Breast Cancer under DifferentRates of Chemoradiotherapy

Project description:Dynamics of Breast Cancer under Different Rates of Chemoradiotherapy. Mkango SB1, Shaban N1, Mureithi E1, Ngoma T2. Author information 1 Department of Mathematics, University of Dar es Salaam, P.O. Box 35062, Dar es Salaam, Tanzania. 2 Department of Clinical Oncology, Muhimbili University of Health and Allied Sciences, P.O. Box 65000, Dar es Salaam, Tanzania. Abstract A type of cancer which originates from the breast tissue is referred to as breast cancer. Globally, it is the most common cause of death in women. Treatments such as radiotherapy, chemotherapy, hormone therapy, immunotherapy, and gene therapy are the main strategies in the fight against breast cancer. The present study aims at investigating the effects of the combined radiotherapy and chemotherapy as a way to treat breast cancer, and different treatment approaches are incorporated into the model. Also, the model is fitted to data on patients with breast cancer in Tanzania. We determine new treatment strategies, and finally, we show that when sufficient amount of chemotherapy and radiotherapy with a low decay rate is used, the drug will be significantly more effective in combating the disease while health cells remain above the threshold. Copyright © 2019 Sara B. Mkango et al.

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Histone methyltransferase PRDM9 promotes survival of drug-tolerant persister cells in glioblastoma [ChIP-seq]

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Histone methyltransferase PRDM9 promotes survival of drug-tolerant persister cells in glioblastoma [ChIP-seq]

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Histone methyltransferase PRDM9 promotes survival of drug-tolerant persister cells in glioblastoma [RNA-seq]

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Histone methyltransferase PRDM9 promotes survival of drug-tolerant persister cells in glioblastoma [RNA-Seq FPW1 DTPs]

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Project description:Chemotherapy often kills a large fraction of cancer cells but leaves behind a small population of drug-tolerant persister cells. These persister cells survive drug treatments through reversible, non-genetic mechanisms and cause tumour recurrence upon cessation of therapy. Here, we report a drug tolerance mechanism regulated by the germ-cell-specific H3K4 methyltransferase PRDM9. Through histone proteomic, transcriptomic, lipidomic, and ChIP-sequencing studies combined with CRISPR knockout and phenotypic drug screen, we identified that chemotherapy-induced PRDM9 upregulation promotes metabolic rewiring in glioblastoma stem cells, leading to chemotherapy tolerance. Mechanistically, PRDM9-dependent H3K4me3 at cholesterol biosynthesis genes enhances cholesterol biosynthesis, which persister cells rely on to maintain homeostasis under chemotherapy-induced oxidative stress and lipid peroxidation. PRDM9 inhibition, combined with chemotherapy, resulted in strong anti-cancer efficacy in preclinical glioblastoma models, significantly enhancing the magnitude and duration of the antitumor response by eliminating persisters. These findings demonstrate a previously unknown role of PRDM9 in promoting metabolic reprogramming that enables the survival of drug-tolerant persister cells.

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