原创力文档adhesion molecule periplakin is involved in cellular movement and attachment in pharyngeal squamous cancer cells粘附分子periplakin参与细胞运动和附件咽鳞状细胞癌细胞.pdfVIP
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adhesion molecule periplakin is involved in cellular movement and attachment in pharyngeal squamous cancer cells粘附分子periplakin参与细胞运动和附件咽鳞状细胞癌细胞
Tonoike et al. BMC Cell Biology 2011, 12:41
/1471-2121/12/41
RESEARCH ARTICLE Open Access
Adhesion molecule periplakin is involved in
cellular movement and attachment in pharyngeal
squamous cancer cells
1,2 2,3* 3,4 1,2 2 5
Yurie Tonoike , Kazuyuki Matsushita , Takeshi Tomonaga , Koji Katada , Nobuko Tanaka , Hideaki Shimada ,
Yukio Nakatani6, Yoshitaka Okamoto1 and Fumio Nomura2,3
Abstract
Background: We previously reported that periplakin (PPL) is downregulated in human esophageal cancer tissues
compared to the adjacent non-cancer epithelium. Thus PPL could be a useful marker for detection of early
esophageal cancer and evaluation of tumor progression, but largely remains unknown in this field. To investigate
PPL involvement in carcinogenesis, tumor progression, cellular movement or attachment activity, siRNAs against
PPL were transfected into pharyngeal squamous cancer cell lines and their effects on cellular behaviours were
examined.
Results: PPL knockdown appeared to decrease tumor cell growth together with G2/M phase accumulation in cells
attached to a culture dish. However, the extent of cell growth suppression, evaluated by the number of cells
attached to the culture dish, was too distinctive to be explained only by cell cycle delay. Importantly, PPL
knockdown suppressed cellular movement and attachment to the culture dish accompanied by decreased
pAktSer473 phosphorylation. Additionally, LY294002, a PI3K inhibitor that dephosphorylates pAktSer473, significantly
suppressed D562 cell migration. Thus PPL potentially engages in cellular movement al least partly via the PI3K/Akt
axis.
Conclusions: PPL knockdown is related to reduced cellular movement and attachment a
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