Wnt/β-catenin Signaling in Lung Cancer: Association with Proliferation, Metastasis, and Therapy Resistance.
Cancer therapy
Chemoresistance
Lung cancer
Metastasis
Wnt/?-catenin
Wnt/?-catenin signaling
Journal
Current cancer drug targets
ISSN: 1873-5576
Titre abrégé: Curr Cancer Drug Targets
Pays: Netherlands
ID NLM: 101094211
Informations de publication
Date de publication:
13 Apr 2023
13 Apr 2023
Historique:
received:
19
07
2022
revised:
30
01
2023
accepted:
22
02
2023
entrez:
18
4
2023
pubmed:
19
4
2023
medline:
19
4
2023
Statut:
aheadofprint
Résumé
The capacity of cancer cells for abnormal growth and metastasis has made it difficult to find a cure for tumor. Both males and females suffer from lung tumors, and physicians still deem them incurable. The initiation and development of lung tumors can be forced by genomic mutations. Wnt is a critical pathway for regulating growth, differentiation and migration. However, its oncogenic function has been observed in lung cancer. Wnt is able to increase the proliferation of lung tumors. The metastasis potential of lung tumors can be accelerated by Wnt/EMT axis. Overexpression of Wnt/β-catenin prevents chemotherapy-mediated cell death in lung tumors. This pathway promotes cancer stem cell features in lung tumors which induce radioresistance. Anti-cancer agents, such as curcumin, are able to inhibit Wnt in lung tumor treatment. Wnt interaction with other factors in lung tumors is essential in controlling biological behavior, and non-coding RNA transcripts are the most well-known ones. It can be concluded from the current study that Wnt is an important regulator of lung tumorigenesis, and the translation of these findings into the clinic is vital.
Identifiants
pubmed: 37069720
pii: CCDT-EPUB-130919
doi: 10.2174/1568009623666230413094317
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.