Molecular landscape of c-Myc signaling in prostate cancer: A roadmap to clinical translation.
Biomarker
C-Myc
Drug resistance
Non-coding RNAs
Prostate cancer
Journal
Pathology, research and practice
ISSN: 1618-0631
Titre abrégé: Pathol Res Pract
Pays: Germany
ID NLM: 7806109
Informations de publication
Date de publication:
May 2022
May 2022
Historique:
received:
29
01
2022
revised:
02
03
2022
accepted:
17
03
2022
pubmed:
28
3
2022
medline:
6
5
2022
entrez:
27
3
2022
Statut:
ppublish
Résumé
The c-Myc signaling is a new emerging target in cancer therapy. Activation of c-Myc signaling leads to cancer growth and invasion in vitro and in vivo. The stability of c-Myc can also mediate drug resistance and radioresistance in cancers. The apoptosis inhibition and enhancing cell cycle progression are mediated by c-Myc overexpression. On the other hand, prostate cancer (PC) is the most common cancer in men and causes high death. The present review focuses on c-Myc signaling in PC. The c-Myc overexpression is in favor of PC growth and migration. Upon c-Myc inhibition, apoptosis and cell cycle arrest (G0/G1 phase) occur in PC cells. The c-Myc induces glycolysis in enhancing PC growth. Besides, stability and overexpression of c-Myc can mediate resistance of PC cells to chemotherapy and radiotherapy. The inhibition of c-Myc by both anti-tumor agents and genetic tools suppress PC progression. The miRNAs, lncRNAs, circRNAs and other factors such as PI3K/Akt can act as upstream regulator of c-Myc signaling. The c-Myc can function as independent prognostic and diagnostic factor in PC patients. The c-Myc upregulation is associated with reduced overall survival, clinical stage, lymph node metastasis and undesirable prognosis of PC patients.
Identifiants
pubmed: 35339914
pii: S0344-0338(22)00094-2
doi: 10.1016/j.prp.2022.153851
pii:
doi:
Substances chimiques
MYC protein, human
0
Proto-Oncogene Proteins c-myc
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
153851Informations de copyright
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