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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Nuclear reprogramming is a process of transforming one cell type into an unrelated cell type by epigenetic changes that alter the cell’s original gene expression pattern. Such epigenetic changes force cells to express a different set of genes, which play a significant role in inducing transformation into other cell types. Nuclear reprogramming offers applications in reproductive cloning for livestock propagation and regenerative medicine — developing patient-specific cells for...
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Serotonin Modulates Lineage Plasticity in Neuroendocrine Prostate Cancer via Epigenetic Reprogramming.

Yiyi Ji1,2, Cheng-Wei Ju3, Lei Chen4

  • 1Department of Urology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

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|December 19, 2025
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Summary
This summary is machine-generated.

Neuroendocrine prostate cancer (NEPC) progression is driven by an internal serotonin pathway. Inhibiting serotonin synthesis with carbidopa effectively reduces tumor growth and improves survival in NEPC models.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Neuroendocrine prostate cancer (NEPC) is an aggressive subtype of prostate cancer known for therapy resistance and lineage plasticity.
  • The role of metabolic and signaling molecules in NEPC cell fate transitions is not fully understood.
  • NE tumors are characterized by the production and accumulation of serotonin, a neurotransmitter with diverse physiological functions.

Purpose of the Study:

  • To investigate the role of a tumor-intrinsic serotonin axis in driving NEPC lineage commitment and progression.
  • To elucidate the molecular mechanisms by which serotonin influences NEPC development.
  • To evaluate the therapeutic potential of targeting the serotonin pathway in NEPC.

Main Methods:

  • Identification of serotonin synthesis and reuptake pathways in NEPC cells, including aromatic L-amino acid decarboxylase (DDC) and SLC6A4.
  • Analysis of the impact of intracellular serotonin on histone modifications, specifically histone serotonylation at H3K4me3Q5.
  • Assessment of downstream gene expression changes and androgen receptor signaling.
  • Pharmacological inhibition of DDC using carbidopa in genetically engineered and patient-derived xenograft models of NEPC.

Main Results:

  • A tumor-intrinsic serotonin axis, involving endogenous serotonin synthesis via DDC and reuptake via SLC6A4, was identified as a key driver of NEPC.
  • High intracellular serotonin levels promote histone serotonylation at H3K4me3Q5, altering the chromatin landscape and gene expression.
  • This epigenetic reprogramming drives NE differentiation and is associated with suppressed androgen receptor signaling.
  • Pharmacological inhibition of DDC with carbidopa significantly reduced tumor growth and prolonged survival in preclinical NEPC models.

Conclusions:

  • The serotonin axis is a critical regulator of NEPC lineage commitment and progression.
  • Histone serotonylation represents a novel, druggable vulnerability in NEPC.
  • Targeting serotonin synthesis with DDC inhibitors like carbidopa shows therapeutic promise for NEPC treatment.