Oropeza-Martínez E, Palacios Serrato EG, Zamora-Salas SX, Lira-Rodríguez NA, López-Mignon SH, Martinez-Benitez MB, Tecalco-Cruz AC. Interferon-gamma signaling pathway: Modulation of key genes in the progression of glioblastoma. World J Biol Chem 2025; 16(4): 112768 [DOI: 10.4331/wjbc.v16.i4.112768]
Corresponding Author of This Article
Angeles C Tecalco-Cruz, PhD, Full Professor, Posgrado en Ciencias Genómicas, Autonomous University of Mexico City, Colonia Del Valle, San Lorenzo 290, Mexico 03100, Ciudad de México, 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 Biol Chem. Dec 5, 2025; 16(4): 112768 Published online Dec 5, 2025. doi: 10.4331/wjbc.v16.i4.112768
Interferon-gamma signaling pathway: Modulation of key genes in the progression of glioblastoma
Enrique Oropeza-Martínez, Eva G Palacios Serrato, Sayra X Zamora-Salas, Norma A Lira-Rodríguez, Sianka’an HZ López-Mignon, Maximo B Martinez-Benitez, Angeles C Tecalco-Cruz
Enrique Oropeza-Martínez, Eva G Palacios Serrato, Sayra X Zamora-Salas, Norma A Lira-Rodríguez, Sianka’an HZ López-Mignon, Maximo B Martinez-Benitez, Angeles C Tecalco-Cruz, Posgrado en Ciencias Genómicas, Autonomous University of Mexico City, Mexico 03100, Ciudad de México, Mexico
Author contributions: Oropeza-Martínez E researched, wrote, and integrated the information in the manuscript and figures; Palacios Serrato EG, Lira-Rodríguez NA, Zamora-Salas SX, López-Mignon SHZ, Martinez-Benitez B researched and wrote some parts of the manuscript; Tecalco-Cruz AC designed this research, discussed, and integrated the manuscript; and all authors approved the final manuscript.
Supported by Colegio de Ciencia y Tecnología de la Universidad Autónoma de la Ciudad de México, No. CCYT-2025-CON-11.
Conflict-of-interest statement: There is no conflict of interest associated with any of the senior authors or other coauthors who contributed their efforts in this manuscript.
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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Angeles C Tecalco-Cruz, PhD, Full Professor, Posgrado en Ciencias Genómicas, Autonomous University of Mexico City, Colonia Del Valle, San Lorenzo 290, Mexico 03100, Ciudad de México, Mexico. angeles.tecalco@uacm.edu.mx
Received: August 5, 2025 Revised: September 8, 2025 Accepted: November 26, 2025 Published online: December 5, 2025 Processing time: 121 Days and 2.5 Hours
Abstract
The canonical signaling of interferon gamma (IFN-γ) through the Janus kinase 1 and 2–signal transducer and activator of transcription 1 (STAT1) axis leads to the expression of several interferon-stimulated genes (ISGs), which have diverse effects depending on the cellular context. In glioblastoma, a highly aggressive primary brain tumor in adults, elements of IFN-γ canonical signaling are deregulated, resulting in the overexpression of STAT1-target ISGs associated with tumor progression. This mini-review highlights key ISGs, including STAT1, interferon regulatory factor 1, programmed death-ligand 1, indoleamine 2,3-dioxygenase 1, and interferon-stimulated gene 15, involved in the pathology of glioblastoma. These genes may serve as valuable biomarkers and have therapeutic potential for targeting IFN-γ signaling in this malignancy.
Core Tip: This review examines the characteristics and functions of five genes induced by interferon-gamma—signal transducer and activator of transcription 1, interferon regulatory factor 1, programmed death-ligand 1, indoleamine 2,3-dioxygenase 1, and interferon-stimulated gene 15—that participate in various mechanisms that promote glioblastoma, a highly aggressive brain tumor; therefore, investigating these genes could contribute to the identification of potential biomarkers and therapeutic targets.
