Reduced lamin a/c does not facilitate cancer cell transendothelial migration but compromises lung metastasis

Francesco Roncato, Ofer Regev, Sara W. Feigelson, Sandeep Kumar Yadav, Lukasz Kaczmarczyk, Nehora Levi, Diana Drago-Garcia, Samuel Ovadia, Marina Kizner, Yoseph Addadi, João C. Sabino, Yossi Ovadya, Sérgio F. de Almeida, Ester Feldmesser, Gabi Gerlitz, Ronen Alon

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


The mechanisms by which the nuclear lamina of tumor cells influences tumor growth and migration are highly disputed. Lamin A and its variant lamin C are key lamina proteins that control nucleus stiffness and chromatin conformation. Downregulation of lamin A/C in two prototypic metastatic lines, B16F10 melanoma and E0771 breast carcinoma, facilitated cell squeezing through rigid pores, and reduced heterochromatin content. Surprisingly, both lamin A/C knockdown cells grew poorly in 3D spheroids within soft agar, and lamin A/C deficient cells derived from spheroids transcribed lower levels of the growth regulator Yap1. Unexpectedly, the transendothelial migration of both cancer cells in vitro and in vivo, through lung capillaries, was not elevated by lamin A/C knockdown and their metastasis in lungs was even dramatically reduced. Our results are the first indication that reduced lamin A/C content in distinct types of highly metastatic cancer cells does not elevate their transendothelial migration (TEM) capacity and diapedesis through lung vessels but can compromise lung metastasis at a post extravasation level.

Original languageEnglish
Article number2383
Issue number10
StatePublished - 2 May 2021


  • Cancer metastasis
  • Chemotaxis
  • Diapedesis
  • Epigenetics
  • Extravasation
  • Imaging
  • Nucleus


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