Calreticulin, an endoplasmic reticulum-resident protein, is highly expressedand essential for cell proliferation and migration in oral squamous cell carcinoma

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Title:	Calreticulin, an endoplasmic reticulum-resident protein, is highly expressedand essential for cell proliferation and migration in oral squamous cell carcinoma
Authors:	Wei-Fan Chiang;Tzer-Zen Hwang;Tzyh-Chyuan Hour;Lee-Hsin Wang;Chien-Chih Chiu;Hau-Ren Chen;Yu-Jen Wu;Chih-Chun Wang;Ling-Feng Wangh;Chen-Yu Chien;Jen-Hao Chen;Chao-Tien Hsu;Jff Yi-Fu Chen
Contributors:	健康暨護理學院
Date:	2013
Issue Date:	2013-10-11T07:54:44Z (UTC)
Abstract:	Oral squamous cell carcinoma (OSCC) has emerged as one of the major malignant tumors of the head and neck cancers. However, the molecular mechanism behind tumorigenesis of OSCC is not fully understood. The aim of this study was to investigate the role of calreticulin (CRT), an endoplasmic reticulum-resident protein, in OSCC cells. Materials and methods: Sixteen paired samples of tumor and non-cancerous matched tissue (NCMT), six OSCC cell lines and normal human oral keratinocytes (NHOKs), and oral tissue microarray were used to reveal the expression of CRT by Western blotting and immunohistochemistry. Later, shRNA-mediated stable knockdown of CRT in OSCC cells was generated. The knockdown cell line was used to analyze cell proliferation, colony formation, anchorage-independent growth and cell migration in vitro. Results: CRT was differentially expressed in fresh tumor samples and six OSCC cell lines but not adjacent NCMTs and NHOKs. In oral tissue microarray, we showed that there was positive CRT staining in the vast majority of tumor cases (99/103), in sharp contrast to that in NCMT cases (29/92) (p < 0.001). Stable knockdown of CRT in oral cancer cells resulted in significantly reduced growth rate, colony-forming capacity and anchorage-independent growth. This may be attributed to the induction of G0/G1 cell cycle arrest when CRT was depleted in the cells. Both horizontal and vertical movements of the CRTknockdown stable line were markedly impaired. The phosphorylation levels of focal adhesion kinase (FAK), paxillin and ERK1/2 and the activity of matrix metalloproteinase-2 and -9 (MMP-2 and MMP-9) were decreased in the CRT-knockdown cells. These results suggest that CRT can regulate oral cancer cell migration through activation of the FAK signaling pathway accompanied with proteolytic degradation of the extracellular matrix (ECM) by MMP-2 and MMP-9. Conclusion: Together, this study has defined a novel biological role for CRT in oral cancer. CRT is a potential biomarker and may contribute to the malignant phenotypes of OSCC cells.
Relation:	Oral Oncology
Appears in Collections:	[Department of Beauty Science] Papers

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