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Review
. 2024 Feb;62(1):e23568.
doi: 10.1002/dvg.23568. Epub 2023 Nov 9.

EMT and primary ciliogenesis: For better or worse in sickness and in health

Camille E Tessier  1 , Aurore M M Dupuy  1 , Thomas Pelé  1 , Philippe P Juin  1   2 , Jacqueline A Lees  3 , Vincent J Guen  1
Affiliations
Review

EMT and primary ciliogenesis: For better or worse in sickness and in health

Camille E Tessier et al. Genesis. 2024 Feb.

Abstract

Epithelial-mesenchymal transition (EMT) and primary ciliogenesis are two cell-biological programs that are essential for development of multicellular organisms and whose abnormal regulation results in many diseases (i.e., developmental anomalies and cancers). Emerging studies suggest an intricate interplay between these two processes. Here, we discuss physiological and pathological contexts in which their interconnections promote normal development or disease progression. We describe underlying molecular mechanisms of the interplay and EMT/ciliary signaling axes that influence EMT-related processes (i.e., stemness, motility and invasion). Understanding the molecular and cellular mechanisms of the relationship between EMT and primary ciliogenesis may provide new insights in the etiology of diseases related to EMT and cilia dysfunction.

Keywords: early development, process; mammal, process; organism; signaling.

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References

REFERENCES

    1. Ahmed, N., Maines‐Bandiera, S., Quinn, M. A., Unger, W. G., Dedhar, S., & Auersperg, N. (2006). Molecular pathways regulating EGF‐induced epithelio‐mesenchymal transition in human ovarian surface epithelium. American Journal of Physiology. Cell Physiology, 290, C1532–C1542. https://doi.org/10.1152/ajpcell.00478.2005
    1. Arnoux, V., Nassour, M., L'Helgoualc'h, A., Hipskind, R. A., & Savagner, P. (2008). Erk5 controls slug expression and keratinocyte activation during wound healing. Molecular Biology of the Cell, 19, 4738–4749. https://doi.org/10.1091/mbc.E07-10-1078
    1. Becker, K. F., Atkinson, M. J., Reich, U., Becker, I., Nekarda, H., Siewert, J. R., & Höfler, H. (1994). E‐cadherin gene mutations provide clues to diffuse type gastric carcinomas. Cancer Research, 54, 3845–3852.
    1. Berx, G., Cleton‐Jansen, A. M., Nollet, F., de Leeuw, W. J., van de Vijver, M., Cornelisse, C., & van Roy, F. (1995). E‐cadherin is a tumour/invasion suppressor gene mutated in human lobular breast cancers. The EMBO Journal, 14, 6107–6115.
    1. Blom, J. N., Wang, X., Lu, X., Kim, M. Y., Wang, G., & Feng, Q. (2022). Inhibition of intraflagellar transport protein‐88 promotes epithelial‐to‐mesenchymal transition and reduces cardiac remodeling post‐myocardial infarction. European Journal of Pharmacology, 933, 175287. https://doi.org/10.1016/j.ejphar.2022.175287

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