The novel epithelial-mesenchymal transition-related proteins and their therapeutic targets in cholangiocarcinoma: a narrative review

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Abstract

Background and Objective

Cholangiocarcinoma (CCA), a liver cancer of bile duct epithelial cells, is a severe health issue in northeastern Thailand. The epithelial-mesenchymal transition (EMT) is a crucial process in the development of CCA. To comprehend oncogenic EMT in CCA, several newly found EMT factors are being explored in these underlying pathways. This narrative review explained the latest in vitro and in vivo findings on the molecular mechanisms of 21 new EMT-related proteins that affect CCA progression.

Methods

We evaluated the PubMed database for relevant articles that fulfilled our criteria for investigating the molecular pathways of the novel EMT markers involved in oncogenic EMT and how they contribute to CCA development, including cell proliferation, apoptosis, invasion, migration, and chemoresistance.

Key Content and Findings

We discuss the potential of these new EMT markers as diagnostic, prognostic, and therapeutic indicators for CCA and describe their underlying mechanisms in the development of the disease. The discovery of several oncogenic EMT proteins and their key signaling pathways and downstream targets will also broaden novel paths of investigation into the diagnosis and targeted treatment of CCA.

Conclusions

The EMT-related proteins that were found are good sources of knowledge and interesting information for future research. The possible ways to treat CCA that could be tested in clinical trials were also discussed.

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Most cited references 91

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The epithelial to mesenchymal transition (EMT) plays crucial roles in the formation of the body plan and in the differentiation of multiple tissues and organs. EMT also contributes to tissue repair, but it can adversely cause organ fibrosis and promote carcinoma progression through a variety of mechanisms. EMT endows cells with migratory and invasive properties, induces stem cell properties, prevents apoptosis and senescence, and contributes to immunosuppression. Thus, the mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.

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The transdifferentiation of epithelial cells into motile mesenchymal cells, a process known as epithelial-mesenchymal transition (EMT), is integral in development, wound healing and stem cell behaviour, and contributes pathologically to fibrosis and cancer progression. This switch in cell differentiation and behaviour is mediated by key transcription factors, including SNAIL, zinc-finger E-box-binding (ZEB) and basic helix-loop-helix transcription factors, the functions of which are finely regulated at the transcriptional, translational and post-translational levels. The reprogramming of gene expression during EMT, as well as non-transcriptional changes, are initiated and controlled by signalling pathways that respond to extracellular cues. Among these, transforming growth factor-β (TGFβ) family signalling has a predominant role; however, the convergence of signalling pathways is essential for EMT.

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Tumorigenesis is dependent on the reprogramming of cellular metabolism as both direct and indirect consequence of oncogenic mutations. A common feature of cancer cell metabolism is the ability to acquire necessary nutrients from a frequently nutrient-poor environment and utilize these nutrients to both maintain viability and build new biomass. The alterations in intracellular and extracellular metabolites that can accompany cancer-associated metabolic reprogramming have profound effects on gene expression, cellular differentiation, and the tumor microenvironment. In this Perspective, we have organized known cancer-associated metabolic changes into six hallmarks: (1) deregulated uptake of glucose and amino acids, (2) use of opportunistic modes of nutrient acquisition, (3) use of glycolysis/TCA cycle intermediates for biosynthesis and NADPH production, (4) increased demand for nitrogen, (5) alterations in metabolite-driven gene regulation, and (6) metabolic interactions with the microenvironment. While few tumors display all six hallmarks, most display several. The specific hallmarks exhibited by an individual tumor may ultimately contribute to better tumor classification and aid in directing treatment.

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Author and article information

Journal

Journal ID (nlm-ta): J Gastrointest Oncol

Journal ID (iso-abbrev): J Gastrointest Oncol

Journal ID (publisher-id): JGO

Title: Journal of Gastrointestinal Oncology

Publisher: AME Publishing Company

ISSN (Print): 2078-6891

ISSN (Electronic): 2219-679X

Publication date (Electronic): 26 May 2023

Publication date (Print): 30 June 2023

Volume: 14

Issue: 3

Pages: 1593-1612

Affiliations

[1 ]deptFaculty of Associated Medical Sciences , Khon Kaen University , Khon Kaen, Thailand;

[2 ]deptCholangiocarcinoma Research Institute , Khon Kaen University , Khon Kaen, Thailand;

[3 ]deptDepartment of Clinical Microbiology, Faculty of Associated Medical Sciences , Khon Kaen University , Khon Kaen, Thailand

Author notes

Contributions: (I) Conception and design: Both authors; (II) Administrative support: A Techasen; (III) Provision of study materials or patients: Both authors; (IV) Collection and assembly of data: P Kimawaha; (V) Data analysis and interpretation: P Kimawaha; (VI) Manuscript writing: Both authors; (VII) Final approval of manuscript: Both authors.

Correspondence to: Anchalee Techasen, PhD. Cholangiocarcinoma Research Institute, Khon Kaen University, Mittraphap Road, Muang Khon Kaen, Khon Kaen 40002, Thailand; Department of Clinical Microbiology, Faculty of Associated Medical Sciences, Khon Kaen University, Khon Kaen 40002, Thailand. Email: anchte@ 123456kku.ac.th .

[^]

ORCID: 0000-0002-4230-5641.

Article

Publisher ID: jgo-14-03-1593

DOI: 10.21037/jgo-22-1126

PMC ID: 10331758

SO-VID: 705ae527-7e47-4bab-a22c-717b781d20f5

License:

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0.

History

Date received : 09 November 2022

Date accepted : 17 May 2023

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The novel epithelial-mesenchymal transition-related proteins and their therapeutic targets in cholangiocarcinoma: a narrative review

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Abstract

Background and Objective

Methods

Key Content and Findings

Conclusions

Related collections

Journal of Circulating Biomarkers

Most cited references 91

Epithelial-mesenchymal transitions in development and disease.

Molecular mechanisms of epithelial-mesenchymal transition.

The Emerging Hallmarks of Cancer Metabolism.

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