EPLIN is a crucial regulator for extrusion of RasV12- transformed cells

Atsuko Ohoka, Mihoko Kajita, Junichi Ikenouchi, Yuta Yako, Sho Kitamoto, Shunsuke Kon, Masaya Ikegawa, Takashi Shimada, Susumu Ishikawa, Yasuyuki Fujita

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35 Citations (Scopus)

Abstract

At the initial stage of carcinogenesis, a mutation occurs in a single cell within a normal epithelial layer. We have previously shown that RasV12-transformed cells are apically extruded from the epithelium when surrounded by normal cells. However, the molecular mechanisms underlying this phenomenon remain elusive. Here, we demonstrate that Cav-1-containing microdomains and EPLIN (also known as LIMA1) are accumulated in RasV12-transformed cells that are surrounded by normal cells. We also show that knockdown of Cav-1 or EPLIN suppresses apical extrusion of RasV12-transformed cells, suggesting their positive role in the elimination of transformed cells from epithelia. EPLIN functions upstream of Cav-1 and affects its enrichment in RasV12-transformed cells that are surrounded by normal cells. Furthermore, EPLIN regulates non-cell-autonomous activation of myosin-II and protein kinase A (PKA) in RasV12-transformed cells. In addition, EPLIN substantially affects the accumulation of filamin A, a vital player in epithelial defense against cancer (EDAC), in the neighboring normal cells, and vice versa. These results indicate that EPLIN is a crucial regulator of the interaction between normal and transformed epithelial cells.

Original languageEnglish
Pages (from-to)781-789
Number of pages9
JournalJournal of cell science
Volume128
Issue number4
DOIs
Publication statusPublished - 2015

All Science Journal Classification (ASJC) codes

  • Cell Biology

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    Ohoka, A., Kajita, M., Ikenouchi, J., Yako, Y., Kitamoto, S., Kon, S., Ikegawa, M., Shimada, T., Ishikawa, S., & Fujita, Y. (2015). EPLIN is a crucial regulator for extrusion of RasV12- transformed cells. Journal of cell science, 128(4), 781-789. https://doi.org/10.1242/jcs.163113