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Targeting the TLK1-MK5 Axis Suppresses Prostate Cancer Metastasis.

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TLK1>Nek1 Axis Promotes Nuclear Retention and Activation of YAP with Implications for Castration-Resistant Prostate Cancer.

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Exploiting TLK1 and Cisplatin Synergy for Synthetic Lethality in Androgen-Insensitive Prostate Cancer.

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Updated: Jun 3, 2025

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
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Beyond the Horizon: Rethinking Prostate Cancer Treatment Through Innovation and Alternative Strategies.

Siddhant Bhoir1,2, Arrigo De Benedetti1

  • 1Department of Biochemistry and Molecular Biology, LSU Health Shreveport, Shreveport, LA 71103, USA.

Cancers
|January 11, 2025
PubMed
Summary

Prostate cancer cells adapt to androgen deprivation therapy by upregulating TLK1B via mTOR signaling. This adaptation promotes survival and resistance, offering a new therapeutic target for advanced prostate cancer.

Keywords:
J54TLK1 inhibitorandrogen receptor signalingprostate cancer (PCa)tousled-like kinase 1 (TLK1) pathway inhibition

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Prostate cancer (PCa) growth is historically linked to androgen receptor (AR) signaling.
  • Therapeutic strategies primarily focus on inhibiting AR signaling.
  • Limited understanding exists regarding cellular responses to AR signaling suppression.

Purpose of the Study:

  • To investigate molecular mechanisms driving PCa adaptation to AR signaling inhibition.
  • To identify novel therapeutic targets in treatment-resistant prostate cancer.

Main Methods:

  • Analysis of gene expression changes following AR signaling inhibition.
  • Investigation of the role of mammalian target of rapamycin (mTOR) pathway.
  • Elucidation of downstream signaling cascades including TLK1B, NEK1, ATR, Chk1, and YAP.

Main Results:

  • Androgen Receptor Signaling Inhibitor (ARSI) treatment increases TLK1B expression through mTOR-mediated translational derepression.
  • This leads to activation of the TLK1 > NEK1 > ATR > Chk1 and NEK1 > YAP signaling axes.
  • These pathways promote cancer cell survival, quiescence, and adaptation to androgen deprivation therapy (ADT), leading to castration-resistant prostate cancer (CRPC).

Conclusions:

  • Suppression of AR signaling creates a novel vulnerability in prostate cancer.
  • The identified TLK1B-mediated pathway represents a potential therapeutic target for overcoming ADT resistance and CRPC progression.