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Journal of Cancer Research and Clinical Oncology

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01.01.2010 | Original Paper

Overexpression of Plk1 promotes malignant progress in human esophageal squamous cell carcinoma

verfasst von: Chunling Zhao, Lei Gong, Wentong Li, Limei Chen

Erschienen in: Journal of Cancer Research and Clinical Oncology | Ausgabe 1/2010

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Abstract

Purpose

Plk1, belonging to a family of serine/threonine kinases, is involved in spindle formation and chromosome segregation during mitosis and therefore, in the regulation of cell cycle. Plk1 was found to be overexpressed in various human tumors. In the present work, we investigated the expression of human esophageal squamous cell carcinoma (ESCC) to determine whether Plk1 has a role in malignant progress.

Methods

Immunohistochemistry and Western blotting were performed to define the expressions of Plk1 in ESCC tissues and normal adjacent tissues. Transfection of cells with small interference RNA, growth suppression assay, and Transwell assay were used to determine the potential role of Plk1 in ESCC malignant progress.

Results

Plk1 was overexpressed in 69.6% of the ESCC tissues. In addition, the extent of Plk1 expression was closely correlated with differentiation grades and invasiveness in ESCC. We also found that the downregulation of endogenous Plk1 in human ESSC cell lines Eca-109 and EC9706 significantly decreased cells proliferation and migrating ability.

Conclusions

Our results show that Plk1 expression is elevated in ESCC tissues and is associated with differentiation grades and invasiveness in ESCC, indicating that overexpression of Plk1 may play an important role in carcinogenesis and malignant progress of ESCC.

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Titel: Overexpression of Plk1 promotes malignant progress in human esophageal squamous cell carcinoma
verfasst von: Chunling Zhao
Lei Gong
Wentong Li
Limei Chen
Publikationsdatum: 01.01.2010
Verlag: Springer-Verlag
Erschienen in: Journal of Cancer Research and Clinical Oncology / Ausgabe 1/2010
Print ISSN: 0171-5216
Elektronische ISSN: 1432-1335
DOI: https://doi.org/10.1007/s00432-009-0630-4

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