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MINI REVIEW article

Front. Immunol.
Sec. Molecular Innate Immunity
Volume 15 - 2024 | doi: 10.3389/fimmu.2024.1482088
This article is part of the Research Topic Application of Multi-omics Analyses in Revealing the Role of Mitochondrial Gene Defects in Disease Progression View all 12 articles

The mechanisms of Pin1 as targets for cancer therapy

Provisionally accepted
Chuanfeng  Liu Chuanfeng Liu 1Lingying  Dan Lingying Dan 1Quan  Li Quan Li 1Ousman  Bajinka Ousman Bajinka 2Xingxing  Yuan Xingxing Yuan 3*
  • 1 Lishui Traditional Chinese Medicine Hospital, Lishui, Zhejiang Province, China
  • 2 University of the Gambia, Serekunda, Gambia
  • 3 Heilongjiang Academy of Traditional Chinese Medicine, Harbin, China

The final, formatted version of the article will be published soon.

    Targeted therapy has considerable promise for the effective eradication of cancer at the primary tumor site prior to subsequent metastasis. Using this therapeutic approach, gaining an understanding of mechanistic cancer models is essential for facilitating the inhibition or suppression of tumor growth. Among different oncogenes and proteins, the protein interacting with never-in-mitosis kinase-1 (Pin1) is particularly important. The interaction between Pin1 and phosphorylated threonine-proline motifs results in significant alterations in protein structure and function. In this review, we provide a comprehensive summary of the processes involving Pin1 and its mechanisms in the context of cancer therapy. Pin1 enhances signaling pathways in a number of different human cancers and plays a pivotal role in the suppressive mechanisms relevant to cancer treatment. It is essential for the regulation of proline-directed phosphorylation and for modulating tumor suppressors. Inhibitors of Pin1, particularly naturally occurring substances, have been found to inhibit the carcinogenic activity of Pin1, and consequently this protein could represent an excellent candidate for novel cancer treatment strategies, offering a valuable therapeutic target in carcinogenesis and treatment resistance.

    Keywords: Pin1 inhibitor, peptidyl-prolyl isomerase, Cis-trans structure, tumorigenesis, Proline, anticancer therapy

    Received: 17 Aug 2024; Accepted: 25 Oct 2024.

    Copyright: © 2024 Liu, Dan, Li, Bajinka and Yuan. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Xingxing Yuan, Heilongjiang Academy of Traditional Chinese Medicine, Harbin, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.