Deciphering the Role of p60AmotL2 in Epithelial Extrusion and Cell Detachment

Author:

Cui Weiyingqi1,Subramani Aravindh1,Fonseca Pedro1,Zhang Yumeng1,Tong Le1,Zhang Yuanyuan1,Egevad Lars1,Lundqvist Andreas1ORCID,Holmgren Lars1

Affiliation:

1. Department of Oncology-Pathology, Bioclinicum J6:20, Solnavägen 30, Karolinska Institutet, 171 64 Stockholm, Sweden

Abstract

Preserving an accurate cell count is crucial for maintaining homeostasis. Apical extrusion, a process in which redundant cells are eliminated by neighboring cells, plays a key role in this regard. Recent studies have revealed that apical extrusion can also be triggered in cells transformed by oncogenes, suggesting it may be a mechanism through which tumor cells escape their microenvironment. In previous work, we demonstrated that p60AmotL2 modulates the E-cadherin function by inhibiting its connection to radial actin filaments. This isoform of AmotL2 is expressed in invasive breast and colon tumors and promotes invasion in vitro and in vivo. Transcriptionally regulated by c-Fos, p60AmotL2 is induced by local stress signals such as severe hypoxia. In this study, we investigated the normal role of p60AmotL2 in epithelial tissues. We found that this isoform is predominantly expressed in the gut, where cells experience rapid turnover. Through time-lapse imaging, we present evidence that cells expressing p60AmotL2 are extruded by their normal neighboring cells. Based on these findings, we hypothesize that tumor cells exploit this pathway to detach from normal epithelia and invade surrounding tissues.

Funder

Swedish Heart and Lung Foundation

Swedish Research Council

Cancerfonden

Radiumhemmets forskningsfonder

Knut och Alicia Wallenberg

PhD scholarship from the Chinese Scholarship Council

Publisher

MDPI AG

Subject

General Medicine

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1. A phenotypic screening approach to target p60AmotL2-expressing invasive cancer cells;Journal of Experimental & Clinical Cancer Research;2024-04-09

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