Notch signaling in the pathogenesis, progression and identification of potential targets for cholangiocarcinoma (Review)

Peeranate Vanaroj; Wanna Chaijaroenkul; Kesara Na-Bangchang

doi:10.3892/mco.2022.2499

Notch signaling in the pathogenesis, progression and identification of potential targets for cholangiocarcinoma (Review)

Mol Clin Oncol. 2022 Mar;16(3):66. doi: 10.3892/mco.2022.2499. Epub 2022 Jan 19.

Authors

Peeranate Vanaroj¹, Wanna Chaijaroenkul¹, Kesara Na-Bangchang^{1

2}

Affiliations

¹ Graduate Program in Bioclinical Sciences, Chulabhorn International College of Medicine, Thammasat University, Pathumthani, 12120 Thailand.
² Center of Excellence in Pharmacology and Molecular Biology of Malaria and Cholangiocarcinoma, Thammasat University, Pathumthani, 12120 Thailand.

Abstract

Cholangiocarcinoma (CCA) is an aggressive type of bile duct cancer that is characterized by a high mortality rate due to its late diagnosis and ineffective treatment. The aim of the present systematic review was to analyze the association between Notch signaling and CCA in terms of its pathogenesis, progression and potential treatment targets. Relevant information was gathered from the PubMed, ScienceDirect and Scopus databases using the search terms 'cholangiocarcinoma' AND 'Notch signaling'. Of the 90 articles identified, 28 fulfilled the eligibility criteria and were included in the analysis. It was concluded that overexpression/upregulation of Notch ligands, such as Jagged1 and Notch receptors (Notch1, Notch2 and Notch3), as well as upregulation of the upstream Notch signaling pathway, promoted CCA development and progression. In addition, downregulation of Notch1 signaling through several possible interventions appears to be a promising strategy for inhibition of CCA development and progression. Therefore, the Notch signaling pathway may be considered as a potential target for CCA control.

Keywords: Notch signaling; Notch1; Notch2; Notch3; cholangiocarcinoma.

Publication types

Review

Grants and funding

Funding: The study was supported by the Research Team Promotion Grant, National Research Council of Thailand (grant no. NRCT 820/2563), Thammasat University (Center of Excellence in Pharmacology and Molecular Biology of Malaria and Cholangiocarcinoma) and Thammasat University Research Fund (contract no. TUFT 65/2564).