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ABSTRACT
The anti-tumor capacity of natural killer (NK) cells heavily relies on their ability to migrate towards their target cells. This process is based on dynamic actinrearrangement, so-called actin treadmilling, andis tightly regulated by proteins such as cofilin-1. The aim of the present study was to identify the role of cofilin-1 (CFL-1) in the migratory behavior of NK cells and to investigate a possible impact of an obesity-associated micromilieu on these cells, as it is known that obesity correlates with various impaired NK cell functions. CFL-1 was knocked-down via transfection of NK-92 cells with respective siRNAs. Obesity associated micromilieu was mimicked by incubation of NK-92 cells with adipocyte-conditioned medium from human preadipocyte SGBS cells or leptin. Effects on CFL-1 levels, the degree of phosphorylation to the inactive pCFL-1 as well as NK-92 cell motility were analyzed. Surprisingly, siRNA-mediated CFL-1 knockdown led to a significant increase of migration, as determined by enhanced velocity and accumulated distance of migration. No effect on CFL-1 nor pCFL-1 expression levels, proportion of phosphorylation and cell migratory behavior could be demonstrated under the influence of an obesity-associated microenvironment. In conclusion, the results indicate a significant effect of a CFL-1 knockdown on NK cell motility.
Acknowledgments
The authors are grateful to S. Möschter and F. Knöfel for technical assistance.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Supplementary material
Supplemental data for this article can be accessed online at https://doi.org/10.1080/08820139.2024.2327327.
Author contributions
Conceptualization, H.K.,M.H. and B.G.; methodology, M.H., J.O., J.F., T.F., M.B., D.Q., I.B. and S.J.B.; analysis, M.H., T.F., M.B., D.Q., I.B., B.G. and S.J.B.; resources, H.K.; project administration, H.K.; writing-original draft preparation, M.H.; writing-review and editing, H.K., I.B.-W. and B.G. All authors have read and agreed to the actual version of the manuscript.