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Chemogenetic Regulation in Reprogrammed Stem Cell-derived Precursor Cells in Treating Neurodegenerative Diseases
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Reprogramming landscape highlighted by dynamic transcriptomes in therapy-induced neuroendocrine differentiation.

Andrew Michael Asberry1, Sheng Liu2,3, Hye Seung Nam1

  • 1Department of Medicinal Chemistry and Molecular Pharmacology, Purdue University, West Lafayette, IN, USA.

Computational and Structural Biotechnology Journal
|November 16, 2022
PubMed
Summary
This summary is machine-generated.

Androgen signaling inhibitors (ASI) for prostate cancer eventually fail, causing cancer cells to develop neuroendocrine features (NED). This study reveals ASI triggers a shift from epithelial to neuroendocrine-like cells, offering a model to develop new treatments.

Keywords:
ASI, androgen signaling inhibitionAndrogen Receptor (AR)CRPC, castration resistant prostate cancerCYCL, cycling likeENZ, enzalutamideEpigeneticsGEMM, genetically engineered mouse modelHNPC, hormone naïve prostate cancerNE, neuroendocrineNED, neuroendocrine differentiationNEL, neuroendocrine likeNEPC, neuroendocrine prostate cancerNeuroendocrine Differentiation (NED)Neuroendocrine Prostate Cancer (NEPC)Single Cell RNA-SeqTF, transcription factorTransdifferentiation

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Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Prostate cancer treatment with androgen signaling inhibitors (ASI) is limited by therapy failure within 1-2 years.
  • ASI resistance can lead to transdifferentiation into androgen receptor (AR)-negative neuroendocrine prostate cancer (NEPC) in 17-25% of patients.
  • The epigenetic mechanisms driving neuroendocrine differentiation (NED) and ASI-induced NED are not well understood.

Purpose of the Study:

  • To elucidate the epigenetic pathways underlying neuroendocrine differentiation (NED) in prostate cancer.
  • To understand the mechanism of ASI therapy-induced NED.
  • To establish a model system for screening potential therapeutic agents against ASI-induced NED.

Main Methods:

  • Utilized a combinatorial single-cell and bulk mRNA sequencing workflow.
  • Performed time-resolved analysis of prostate cancer cells after enzalutamide treatment.
  • Employed CUT&RUN analysis alongside scRNA-seq.

Main Results:

  • Prostate cancer cells showed immediate loss of canonical AR signaling and morphological changes to neuroendocrine-like (NEL) after AR inhibition.
  • Activation of neuroendocrine (NE)-associated pathways occurred before complete repression of epithelial or AR pathways.
  • ASI therapy induces NED via morphological change, AR target gene deactivation, and NE-associated gene de-repression, while retaining AR expression and non-canonical AR activity.

Conclusions:

  • ASI therapy drives prostate cancer cell transdifferentiation into NEPC through a specific sequence of molecular and morphological events.
  • The observed heterogeneous AR status in clinical samples aligns with the proposed mechanistic model.
  • The developed model system provides a platform for identifying novel therapies to prevent or reverse ASI-induced NED.