Overexpression of cyclin B1 in human esophageal squamous cell carcinoma cells induces tumor cell invasive growth and metastasis

Yongmei Song, Chunling Zhao, Lijia Dong, Ming Fu, Liyan Xue, Zhen Huang, Tong Tong, Zhuan Zhou, Amei Chen, Zhihua Yang, Ning Lu, Qimin Zhan*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

72 Scopus citations

Abstract

Cyclin B1, a key component in the control of cell cycle progression from G2 to M phase, has been implicated in tumorigenesis and the development of malignancy. However, the underlying mechanism by which cyclin B1 acts as an important oncogenic molecule remains largely unknown. Here we show that ectopic expression of cyclin B1 promotes cell proliferation, enhances cell motility and migration and results in increased ability of cells extravasating through the capillary endothelium. Interestingly, isogenic esophageal squamous cell carcinoma (ESCC) cells overexpressing cyclin B1 reveal strong invasive growth and high potential of metastasis to lung in xenograft mice. Suppression of cyclin B1 expression via small interfering RNA approach in high-metastatic esophagus carcinoma cells specifically inhibits their ability to metastasize from the primary ESCC to lung. Notably, altered expression of epithelial markers and mesenchymal markers were observed in the cells overexpressing cyclin B1, suggesting that cyclin B1 contributes to metastasis probably by promoting an epithelial-mesenchymal transition. These results establish a mechanistic link between cyclin B1 and ESCC metastasis and provide novel insight into understanding of cyclin B1 in the development of ESCC malignancy.

Original languageEnglish (US)
Pages (from-to)307-315
Number of pages9
JournalCarcinogenesis
Volume29
Issue number2
DOIs
StatePublished - Feb 2008

ASJC Scopus subject areas

  • Cancer Research

Fingerprint Dive into the research topics of 'Overexpression of cyclin B1 in human esophageal squamous cell carcinoma cells induces tumor cell invasive growth and metastasis'. Together they form a unique fingerprint.

Cite this