A brain-body feedback loop driving HPA-axis dysfunction in breast cancer Article Swipe
Adrian M. Gomez
,
Yue Wu
,
Chao Zhang
,
Leah Boyd
,
Tse-Luen Wee
,
Joseph Gewolb
,
Corina Amor
,
Lucas Cheadle
,
Jeremy C. Borniger
·
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1101/2024.09.13.612923
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1101/2024.09.13.612923
Breast cancer patients often exhibit disrupted circadian rhythms in circulating glucocorticoids (GCs), such as cortisol. This disruption correlates with reduced quality of life and higher cancer mortality 1–3 . The exact cause of this phenomenon — whether due to treatments, stress, age, co-morbidities, lifestyle factors, or the cancer itself remains unclear. Here, we demonstrate that primary breast cancer alone blunts host GC rhythms by disinhibiting neurons in the hypothalamus, and that circadian phase-specific neuromodulation of these neurons can attenuate tumor growth by enhancing anti-tumor immunity. We find that mice with mammary tumors exhibit blunted GC rhythms before tumors are palpable, alongside increased activity in paraventricular hypothalamic neurons expressing corticotropin-releasing hormone (i.e., PVN CRH neurons). Tumor-bearing mice have fewer inhibitory synapses contacting PVN CRH neurons and reduced miniature inhibitory post-synaptic current (mIPSC) frequency, leading to net excitation. Tumor-bearing mice experience impaired negative feedback on GC production, but adrenal and pituitary gland functions are largely unaffected, indicating that alterations in PVN CRH neuronal activity are likely a primary cause of hypothalamic-pituitary-adrenal (HPA) axis dysfunction in breast cancer. Using chemogenetics (hM3Dq) to stimulate PVN CRH neurons at different circadian phases, we show that stimulation just before the light-to-dark transition restores normal GC rhythms and reduces tumor progression. These mice have significantly more effector T cells (CD8+) within the tumor than non-stimulated controls, and the anti-tumor effect of PVN CRH neuronal stimulation is absent in mice lacking CD8+ T cells. Our findings demonstrate that breast cancer distally regulates neurons in the hypothalamus that control output of the HPA axis and provide evidence that therapeutic targeting of these neurons could mitigate tumor progression.
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Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1101/2024.09.13.612923
- OA Status
- green
- Cited By
- 3
- References
- 61
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- OpenAlex ID
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All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4402664258Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1101/2024.09.13.612923Digital Object Identifier
- Title
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A brain-body feedback loop driving HPA-axis dysfunction in breast cancerWork title
- Type
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preprintOpenAlex work type
- Language
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enPrimary language
- Publication year
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2024Year of publication
- Publication date
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2024-09-14Full publication date if available
- Authors
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Adrian M. Gomez, Yue Wu, Chao Zhang, Leah Boyd, Tse-Luen Wee, Joseph Gewolb, Corina Amor, Lucas Cheadle, Jeremy C. BornigerList of authors in order
- Landing page
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https://doi.org/10.1101/2024.09.13.612923Publisher landing page
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YesWhether a free full text is available
- OA status
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greenOpen access status per OpenAlex
- OA URL
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https://www.ncbi.nlm.nih.gov/pmc/articles/11419152Direct OA link when available
- Concepts
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Internal medicine, Endocrinology, Circadian rhythm, Hypothalamus, Breast cancer, Stimulation, Cancer, Hormone, Biology, MedicineTop concepts (fields/topics) attached by OpenAlex
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3Total citation count in OpenAlex
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2025: 3Per-year citation counts (last 5 years)
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10Other works algorithmically related by OpenAlex
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