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Updated: Jun 6, 2025

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The mechanisms of Pin1 as targets for cancer therapy

Chuanfeng Liu1, Lingying Dan2, Quan Li1

  • 1Department of Pulmonary and Critical Care Medicine, Lishui Hospital of Traditional Chinese Medicine, Lishui, China.

Frontiers in Immunology
|December 3, 2024
PubMed

Insights

Targeted cancer therapy shows promise by inhibiting tumor growth. Protein interacting with never-in-mitosis kinase-1 (Pin1) is a key target, as inhibiting its carcinogenic activity offers novel treatment strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Targeted therapy aims to eradicate cancer at the primary site before metastasis.
  • Understanding mechanistic cancer models is crucial for inhibiting tumor growth.
  • The protein interacting with never-in-mitosis kinase-1 (Pin1) is a significant factor in cancer progression.

Purpose of the Study:

  • To provide a comprehensive summary of Pin1's mechanisms in cancer therapy.
  • To highlight Pin1's role in enhancing signaling pathways in various human cancers.
  • To explore Pin1 as a therapeutic target for novel cancer treatment strategies.

Main Methods:

  • Review of existing literature on Pin1 function in cancer.
  • Analysis of Pin1's interaction with phosphorylated threonine-proline motifs.
  • Examination of Pin1's role in regulating proline-directed phosphorylation and tumor suppressors.

Main Results:

  • Pin1 interaction alters protein structure and function, enhancing cancer signaling pathways.
  • Pin1 is essential for regulating proline-directed phosphorylation and modulating tumor suppressors.
  • Naturally occurring Pin1 inhibitors demonstrate efficacy in suppressing carcinogenic activity.

Conclusions:

  • Pin1 plays a pivotal role in cancer suppressive mechanisms and treatment resistance.
  • Pin1 inhibitors represent a promising therapeutic strategy for novel cancer treatments.
  • Targeting Pin1 offers a valuable approach for intervention in carcinogenesis and overcoming treatment resistance.
Keywords:
Pin1 inhibitoranticancer therapycis-trans structurepeptidyl-prolyl isomeraseprolinetumorigenesis

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