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Review
. 2022 Oct 13;10(1):74.
doi: 10.1186/s40364-022-00418-9.

The Wnt/β-catenin signalling pathway in Haematological Neoplasms

Siwei Yu  1 , Ruyue Han  1 , Runliang Gan  2
Affiliations
Review

The Wnt/β-catenin signalling pathway in Haematological Neoplasms

Siwei Yu et al. Biomark Res. .

Abstract

Leukaemia and lymphoma are common malignancies. The Wnt pathway is a complex network of proteins regulating cell proliferation and differentiation, as well as cancer development, and is divided into the Wnt/β-catenin signalling pathway (the canonical Wnt signalling pathway) and the noncanonical Wnt signalling pathway. The Wnt/β-catenin signalling pathway is highly conserved evolutionarily, and activation or inhibition of either of the pathways may lead to cancer development and progression. The aim of this review is to analyse the mechanisms of action of related molecules in the Wnt/β-catenin pathway in haematologic malignancies and their feasibility as therapeutic targets.

Keywords: Haematologic neoplasms; Leukaemia; Lymphoma; Multiple myeloma; Wnt/β-catenin signalling pathway.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Fig. 1
Fig. 1
Regulation of the Wnt/β-catenin signalling pathway. (* As shown in the picture, Wnt signalling is divided into two states: on and off. In the off state, β-catenin in the cytoplasm is phosphorylated by the disruption complex with AXIN as the main scaffold and subsequently presented to the E3 ubiquitin ligase β-TrCP for ubiquitination and degradation. When Wnt ligands bind to FZD-LRP5/6 on the cell membrane, the disruption complex is recruited to the cell membrane. At this point, β-catenin cannot be phosphorylated and occupies the disruption complex, resulting in the accumulation of newly generated β-catenin in the cytoplasm, which then enters the nucleus to regulate TCF/LEF transcription by the action of related molecules)
See this image and copyright information in PMC

References

    1. Rochford R, Cannon MJ, Moormann AM. Endemic Burkitt’s lymphoma: a polymicrobial disease? Nat Rev Microbiol. 2005;3(2):182–7. doi: 10.1038/nrmicro1089. - DOI - PubMed
    1. Gonzalez-Herrero I, Rodriguez-Hernandez G, Luengas-Martinez A, Isidro-Hernandez M, Jimenez R, Garcia-Cenador MB, et al. The Making of Leukemia. Int J Mol Sci. 2018;19(5). DOI:10.3390/ijms19051494. - PMC - PubMed
    1. Kumar SK, Rajkumar V, Kyle RA, van Duin M, Sonneveld P, Mateos MV, et al. Multiple myeloma. Nat Rev Dis Primers. 2017;3:17046. doi: 10.1038/nrdp.2017.46. - DOI - PubMed
    1. Nusse R, Varmus HE. Wnt genes. Cell. 1992;69(7):1073–87. doi: 10.1016/0092-8674(92)90630-u. - DOI - PubMed
    1. Vleminckx K, Wong E, Guger K, Rubinfeld B, Polakis P, Gumbiner BM. Adenomatous polyposis coli tumor suppressor protein has signaling activity in Xenopus laevis embryos resulting in the induction of an ectopic dorsoanterior axis. J Cell Biol. 1997;136(2):411–20. doi: 10.1083/jcb.136.2.411. - DOI - PMC - PubMed

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