Sonic Hedgehog signaling pathway as a potential target to inhibit the progression of hepatocellular carcinoma.
cancer stem cells
hepatocellular carcinoma
recurrence
sonic hedgehog signaling pathway
Journal
Oncology letters
ISSN: 1792-1074
Titre abrégé: Oncol Lett
Pays: Greece
ID NLM: 101531236
Informations de publication
Date de publication:
Nov 2019
Nov 2019
Historique:
received:
09
11
2018
accepted:
06
08
2019
entrez:
16
10
2019
pubmed:
16
10
2019
medline:
16
10
2019
Statut:
ppublish
Résumé
Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-associated mortality worldwide. Hepatocarcinogenesis involves numerous interlinked factors and processes, including the Sonic hedgehog (Shh) signaling pathway, which participates in the carcinogenesis, progression, invasiveness, recurrence and cancer stem cell maintenance of HCC. The Shh signaling pathway is activated by ligands that bind to their receptor protein, Protein patched homolog (Ptch). The process of Shh ligand binding to Ptch weakens the inhibition of smoothened homolog (SMO) and activates signal transduction via glioma-associated oncogene homolog (Gli) transcription factors. The overexpression of Shh pathway molecules, including Shh, Ptch-1, Gli and SMO has been indicated in patients with HCC. It has also been suggested that the Shh signaling pathway exhibits cross-talk between numerous other signaling pathways. The inactivation of the Shh signaling pathway reduces HCC growth, increases radio-sensitivity and increases the beneficial effect of chemotherapy in HCC treatment. Therefore, inhibition of the Shh pathway may be an effective target therapy that can be used in the treatment of HCC.
Identifiants
pubmed: 31611946
doi: 10.3892/ol.2019.10826
pii: OL-0-0-10826
pmc: PMC6781692
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
4377-4384Informations de copyright
Copyright: © Jeng et al.
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