Tecalco-Cruz AC, Abraham-Juárez MJ, Solleiro-Villavicencio H, Ramírez-Jarquín JO. TRIM25: A central factor in breast cancer. World J Clin Oncol 2021; 12(8): 646-655 [PMID: 34513598 DOI: 10.5306/wjco.v12.i8.646]
Corresponding Author of This Article
Angeles C Tecalco-Cruz, PhD, Full Professor, Posgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México (UACM), Colonia Del valle, San Lorenzo 290, Mexico 03100, Mexico. angeles.tecalco@uacm.edu.mx
Research Domain of This Article
Biochemistry & Molecular Biology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Clin Oncol. Aug 24, 2021; 12(8): 646-655 Published online Aug 24, 2021. doi: 10.5306/wjco.v12.i8.646
TRIM25: A central factor in breast cancer
Angeles C Tecalco-Cruz, María Jazmin Abraham-Juárez, Helena Solleiro-Villavicencio, Josué Orlando Ramírez-Jarquín
Angeles C Tecalco-Cruz, Helena Solleiro-Villavicencio, Posgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México (UACM), Mexico 03100, Mexico
María Jazmin Abraham-Juárez, Laboratorio Nacional de Genómica para la Biodiversidad (LANGEBIO), Unidad de Genómica Avanzada, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV-IPN), Irapuato 36821, Mexico
Josué Orlando Ramírez-Jarquín, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico 04510, Mexico
Author contributions: Tecalco-Cruz AC planned the study, participated in the research, organization of this article, and wrote the manuscript; Abraham–Juárez MJ, Solleiro–Villavicencio H and Ramírez-Jarquín JO participated in the research, wrote some part of the manuscript, and prepared some figures of this article.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Angeles C Tecalco-Cruz, PhD, Full Professor, Posgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México (UACM), Colonia Del valle, San Lorenzo 290, Mexico 03100, Mexico. angeles.tecalco@uacm.edu.mx
Received: February 1, 2021 Peer-review started: February 1, 2021 First decision: March 31, 2021 Revised: April 2, 2021 Accepted: July 27, 2021 Article in press: July 27, 2021 Published online: August 24, 2021
Abstract
TRIM25 is emerging as a central factor in breast cancer due to its regulation and function. In particular, it has been shown that: (1) Estrogens modulate TRIM25 gene expression; (2) TRIM25 has activity as an E3-ligase enzyme for ubiquitin; and (3) TRIM25 is also an E3 ligase for interferon-stimulated gene 15 protein in the ISGylation system. Consequently, the proteome of mammary tissue is affected by TRIM25-associated pathways, involved in tumor development and metastasis. Here, we discuss the findings on the mechanisms involved in regulating TRIM25 expression and its functional relevance in breast cancer progression. These studies suggest that TRIM25 may be a biomarker and a therapeutic target for breast cancer.
Core Tip: TRIM25 is an E3-ligase enzyme for the ubiquitination and ISGylation system. TRIM25 expression is deregulated in breast cancer. The activity of TRIM25 is associated with changes in the proteome of mammary tumors. The molecular mechanisms of modulation and action of TRIM25 are implicated in breast cancer progression.
