Sie befinden Sich nicht im Netzwerk der Universität Paderborn. Der Zugriff auf elektronische Ressourcen ist gegebenenfalls nur via VPN oder Shibboleth (DFN-AAI) möglich. mehr Informationen...
Ergebnis 18 von 308

Details

Autor(en) / Beteiligte
Titel
The Interaction Between Autophagy and JAK/STAT3 Signaling Pathway in Tumors
Ist Teil von
  • Frontiers in genetics, 2022-04, Vol.13, p.880359-880359
Ort / Verlag
Switzerland: Frontiers Media S.A
Erscheinungsjahr
2022
Link zum Volltext
Quelle
EZB Electronic Journals Library
Beschreibungen/Notizen
  • Tumor is one of the important factors affecting human life and health in today's world, and scientists have studied it extensively and deeply, among which autophagy and JAK/STAT3 signaling pathway are two important research directions. The JAK/STAT3 axis is a classical intracellular signaling pathway that assumes a key role in the regulation of cell proliferation, apoptosis, and vascular neogenesis, and its abnormal cell signaling and regulation are closely related to the occurrence and development of tumors. Therefore, the JAK/STAT3 pathway in tumor cells and various stromal cells in their microenvironment is often considered as an effective target for tumor therapy. Autophagy is a process that degrades cytoplasmic proteins and organelles through the lysosomal pathway. It is a fundamental metabolic mechanism for intracellular degradation. The mechanism of action of autophagy is complex and may play different roles at various stages of tumor development. Altered STAT3 expression has been found to be accompanied by the abnormal autophagy activity in many oncological studies, and the two may play a synergistic or antagonistic role in promoting or inhibiting the occurrence and development of tumors. This article reviews the recent advances in autophagy and its interaction with JAK/STAT3 signaling pathway in the pathogenesis, prevention, diagnosis, and treatment of tumors.
Sprache
Englisch
Identifikatoren
ISSN: 1664-8021
eISSN: 1664-8021
DOI: 10.3389/fgene.2022.880359
Titel-ID: cdi_doaj_primary_oai_doaj_org_article_dd7ccd3d4c414b00be9387e02ee70533

Weiterführende Literatur

Empfehlungen zum selben Thema automatisch vorgeschlagen von bX