A multi-omics approach to reveal critical mechanisms of activator protein 1 (AP-1)

Li, Fei; Tian, Jiaqi; Zhang, Lin; He, Huan; Song, Dandan

doi:10.1016/j.biopha.2024.117225

Biomedicine & Pharmacotherapy

2024

DOI: 10.1016/j.biopha.2024.117225

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A multi-omics approach to reveal critical mechanisms of activator protein 1 (AP-1)

Fei Li,

Jiaqi Tian,

Lin Zhang

et al.

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Cited by 3 publications

References 78 publications

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FOS‐Mediated PLCB1 Induces Radioresistance and Weakens the Antitumor Effects of CD8⁺ T Cells in Triple‐Negative Breast Cancer

Shu,

Lan,

Luo

et al. 2024

Molecular Carcinogenesis

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Radioresistance and immune evasion are interactive and crucial events leading to treatment failure and progression of human malignancies. This research studies the role of phospholipase C beta 1 (PLCB1) in these events in triple‐negative breast cancer (TNBC) and the regulatory mechanism. PLCB1 was bioinformatically predicted as a dysregulated gene potentially linked to radioresistance in TNBC. Parental TNBC cell lines were exposed to fractionated radiation for 6 weeks. PLCB1 expression was decreased in the first 2 weeks but gradually increased from Week 3. PLCB1 knockdown increased the radiosensitivity of the cells, as manifested by a decreased half‐inhibitory dose of irradiation, reduced cell proliferation, apoptosis resistance, mobility, and tumorigenesis in mice. The FOS transcription factor promoted PLCB1 transcription and activated the PI3K/AKT signaling. Knockdown of FOS similarly reduced radioresistance and T cells‐mediated immune evasion. However, the radiosensitivity of TNBC cells and the antitumor effects of CD8+ T cells could be affected by a PI3K/AKT activator or by the PLCB1 upregulation. The PLCB1 or FOS knockdown also suppressed radioresistance and tumorigenesis of the TNBC cells in mice. In conclusion, FOS‐mediated PLCB1 induces radioresistance and weakens the antitumor effects of CD8+ T cells in TNBC by activating the PI3K/AKT signaling pathway.

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FOS‐Mediated PLCB1 Induces Radioresistance and Weakens the Antitumor Effects of CD8⁺ T Cells in Triple‐Negative Breast Cancer

Shu,

Lan,

Luo

et al. 2024

Molecular Carcinogenesis

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How PPAR-alpha mediated inflammation may affect the pathophysiology of chronic kidney disease

Masenga,

Desta,

Hatcher

et al. 2025

Current Research in Physiology

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Integrating Signaling Pathways with Transcription Factor Networks—On the Trail of Sisyphus?

Papavassiliou,

Papavassiliou

2024

Biomolecules

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A multi-omics approach to reveal critical mechanisms of activator protein 1 (AP-1)

Cited by 3 publications

References 78 publications

FOS‐Mediated PLCB1 Induces Radioresistance and Weakens the Antitumor Effects of CD8⁺ T Cells in Triple‐Negative Breast Cancer

FOS‐Mediated PLCB1 Induces Radioresistance and Weakens the Antitumor Effects of CD8⁺ T Cells in Triple‐Negative Breast Cancer

How PPAR-alpha mediated inflammation may affect the pathophysiology of chronic kidney disease

Integrating Signaling Pathways with Transcription Factor Networks—On the Trail of Sisyphus?

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A multi-omics approach to reveal critical mechanisms of activator protein 1 (AP-1)

Cited by 3 publications

References 78 publications

FOS‐Mediated PLCB1 Induces Radioresistance and Weakens the Antitumor Effects of CD8+ T Cells in Triple‐Negative Breast Cancer

FOS‐Mediated PLCB1 Induces Radioresistance and Weakens the Antitumor Effects of CD8+ T Cells in Triple‐Negative Breast Cancer

How PPAR-alpha mediated inflammation may affect the pathophysiology of chronic kidney disease

Integrating Signaling Pathways with Transcription Factor Networks—On the Trail of Sisyphus?

Contact Info

Product

Resources

About

FOS‐Mediated PLCB1 Induces Radioresistance and Weakens the Antitumor Effects of CD8⁺ T Cells in Triple‐Negative Breast Cancer

FOS‐Mediated PLCB1 Induces Radioresistance and Weakens the Antitumor Effects of CD8⁺ T Cells in Triple‐Negative Breast Cancer