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Open Access Research article

Adhesion molecule periplakin is involved in cellular movement and attachment in pharyngeal squamous cancer cells

Yurie Tonoike12, Kazuyuki Matsushita23*, Takeshi Tomonaga34, Koji Katada12, Nobuko Tanaka2, Hideaki Shimada5, Yukio Nakatani6, Yoshitaka Okamoto1 and Fumio Nomura23

Author Affiliations

1 Department of Otorhinolaryngology, Chiba University Hospital, 1-8-1 Inohana, Chiba City, Chiba 260-8670, Japan

2 Department of Molecular Diagnosis, Graduate School of Medicine, Chiba University Hospital, 1-8-1 Inohana, Chiba City, Chiba 260-8670, Japan

3 Department of Clinical Proteomics Research Center, Chiba University Hospital, 1-8-1 Inohana, Chiba City, Chiba 260-8670, Japan

4 Proteome Research Center, Proteome Research Project, National Institute of Biomedical Innovation, 7-6-8 Saito-Asagi, Ibaraki City, Osaka 567-0085, Japan

5 Department of General and Gastrointestinal Surgery, Toho University Omori Medical Center, 6-11-1 Ohta-ku, Ohmori-nishi, Tokyo 143-8541, Japan

6 Department of Diagnostic Pathology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chiba City, Chiba 260-8670, Japan

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BMC Cell Biology 2011, 12:41  doi:10.1186/1471-2121-12-41

Published: 27 September 2011

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 activity in association with PI3K/Akt axis suppression, rather than malignant progression in pharyngeal cancer cells.