Suscribirse

Research advances in signaling pathways related to the malignant progression of HSIL to invasive cervical cancer: A review - 08/11/24

Doi : 10.1016/j.biopha.2024.117483 
Huifang Wang a, 1, Chang Liu b, c, d, e, 1, Keer Jin b, c, e, Xiang Li e, Jiaxin Zheng e, Danbo Wang b, c, e,
a Department of Obstetrics and Gynecology, Quanzhou Medical College, Quanzhou, Fujian 362010, China 
b Department of Gynecology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang 110042, China 
c Key Clinical Specialty of Liaoning Province, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang 110042, China 
d Central Laboratory, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang 110042, China 
e Department of Gynecology, Cancer Hospital of Dalian University of Technology, Liaoning Cancer Hospital & Institute, Shenyang 110042, China 

Corresponding author at: Department of Gynecology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang 110042, China.Department of Gynecology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & InstituteShenyang110042China

Abstract

The progression of high-grade squamous intraepithelial lesion (HSIL) to invasive cervical cancer (ICC) is a complex process involving persistent human papillomavirus (HPV) infection and changes in signal transduction regulation, energy and material metabolism, cell proliferation, autoimmune, and other biological process in vaginal microenvironment and immune microenviroment. Signaling pathways are a series of interacting molecules in cells that regulate various physiological functions of cells, such as growth, differentiation, metabolism, and death. In the progression of HSIL to ICC, abnormal activation or inhibition in signaling pathways plays an essensial role. This review presented some signaling pathways related to the malignant progression of HSIL to ICC, including p53, Rb, PI3K/AKT/mTOR, Wnt/β-catenin, Notch, NF-κB, MAPK, TGF-β, JAK-STAT, Hippo, and Hedgehog. The molecular mechanisms involved in the biological process of pathway regulation were also analyzed, in order to illustrate the molecular pathway of HSIL progression to ICC and provide references for the development of more effective prevention and treatment methods.

El texto completo de este artículo está disponible en PDF.

Graphical Abstract




 : 

In the study of the molecular mechanisms underlying the progression of high-grade squamous intraepithelial lesions (HSIL) to invasive cervical cancer (ICC), we focused on analyzing and elucidating the roles of signaling pathways such as p53, Rb, PI3K/AKT/mTOR, Wnt/β - catenin, Notch, NF - κ B, MAPK, TGF - β, JAK-STAT, Hippo, and Hedgehog in the malignant transformation of HSIL. Among them, the regulation of p53 and Rb signaling pathways plays a central role in HSIL carcinogenesis. The study revealed that these pathways jointly promote the malignant transformation of lesions by regulating key biological processes such as cell proliferation, apoptosis, invasion, and immune escape, and there are intersections between each pathway.


In the study of the molecular mechanisms underlying the progression of high-grade squamous intraepithelial lesions (HSIL) to invasive cervical cancer (ICC), we focused on analyzing and elucidating the roles of signaling pathways such as p53, Rb, PI3K/AKT/mTOR, Wnt/β - catenin, Notch, NF - κ B, MAPK, TGF - β, JAK-STAT, Hippo, and Hedgehog in the malignant transformation of HSIL. Among them, the regulation of p53 and Rb signaling pathways plays a central role in HSIL carcinogenesis. The study revealed that these pathways jointly promote the malignant transformation of lesions by regulating key biological processes such as cell proliferation, apoptosis, invasion, and immune escape, and there are intersections between each pathway.

El texto completo de este artículo está disponible en PDF.

Keywords : Invasive cervical cancer, High grade squamous intraepithelial lesion, Signaling pathways, Human papillomavirus, Tumor microenvironment


Esquema


© 2024  The Authors. Publicado por Elsevier Masson SAS. Todos los derechos reservados.
Añadir a mi biblioteca Eliminar de mi biblioteca Imprimir
Exportación

    Exportación citas

  • Fichero

  • Contenido

Vol 180

Artículo 117483- novembre 2024 Regresar al número
Artículo precedente Artículo precedente
  • Potential therapeutic application and mechanism of gut microbiota-derived extracellular vesicles in polycystic ovary syndrome
  • Liangliang Yang, Tingxiu Liu, Yan Liao, Yuehan Ren, Zheng Zheng, Mingyue Zhang, Yue Yu, Chang Liu, Chaoying Wang, Tong Chen, Lili Zhang, Dongxue Zheng, Haidan Zhao, Zhexin Ni, Xinmin Liu
| Artículo siguiente Artículo siguiente
  • Advances in stimuli-responsive gold nanorods for drug-delivery and targeted therapy systems
  • Sakineh Hajebi, Mohsen Chamanara, Shadi Sadat Nasiri, Mahsa Ghasri, Alireza Mouraki, Reza Heidari, Abbas Nourmohammadi

Bienvenido a EM-consulte, la referencia de los profesionales de la salud.
El acceso al texto completo de este artículo requiere una suscripción.

¿Ya suscrito a @@106933@@ revista ?

Mi cuenta


Declaración CNIL

EM-CONSULTE.COM se declara a la CNIL, la declaración N º 1286925.

En virtud de la Ley N º 78-17 del 6 de enero de 1978, relativa a las computadoras, archivos y libertades, usted tiene el derecho de oposición (art.26 de la ley), el acceso (art.34 a 38 Ley), y correcta (artículo 36 de la ley) los datos que le conciernen. Por lo tanto, usted puede pedir que se corrija, complementado, clarificado, actualizado o suprimido información sobre usted que son inexactos, incompletos, engañosos, obsoletos o cuya recogida o de conservación o uso está prohibido.
La información personal sobre los visitantes de nuestro sitio, incluyendo su identidad, son confidenciales.
El jefe del sitio en el honor se compromete a respetar la confidencialidad de los requisitos legales aplicables en Francia y no de revelar dicha información a terceros.


Todo el contenido en este sitio: Copyright © 2025 Elsevier, sus licenciantes y colaboradores. Se reservan todos los derechos, incluidos los de minería de texto y datos, entrenamiento de IA y tecnologías similares. Para todo el contenido de acceso abierto, se aplican los términos de licencia de Creative Commons.