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Updated: May 10, 2026

Co-immunoprecipitation Assay for Studying Functional Interactions Between Receptors and Enzymes
09:40

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Published on: September 28, 2018

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Pin1 as a central node in oncogenic signaling: Mechanistic insights and clinical prospects (Review)

Shuning Lei1, Min Luo1, Yuxue Wang1

  • 1Department of Laboratory Medicine, Hubei University of Chinese Medicine, Wuhan, Hubei 430065, P.R. China.

Molecular Medicine Reports
|January 31, 2025
PubMed

Insights

Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (Pin1) regulates cell cycle, proliferation, and apoptosis. Pin1

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (Pin1) is a key regulator of cellular processes.
  • Pin1's role in cell cycle, proliferation, and apoptosis is critical in both normal physiology and pathology.
  • Aberrant Pin1 activity is implicated in various cancers.

Purpose of the Study:

  • To elucidate the mechanistic role of Pin1 in tumorigenesis.
  • To review recent advancements in understanding Pin1's function in cancer development.
  • To explore Pin1 as a potential diagnostic biomarker and therapeutic target in oncology.

Main Methods:

  • Literature review of studies on Pin1 function in cancer.
  • Analysis of Pin1's involvement in cell cycle regulation, signaling pathways, and tumor suppressor functions.
  • Examination of the correlation between Pin1 expression and cancer prognosis.

Main Results:

  • Pin1 promotes cancer cell proliferation and metastasis by modulating the cell cycle and signaling pathways.
  • Upregulated Pin1 expression is linked to poor prognosis across multiple cancer types.
  • Pin1 influences the function of critical tumor suppressors.

Conclusions:

  • Pin1 is a significant factor in tumor initiation and progression.
  • Pin1 represents a promising biomarker for cancer diagnosis and prognosis.
  • Pin1 emerges as a potential therapeutic target for anticancer strategies.
Keywords:
Pin1apoptosiscell cyclesignalingtumor

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