The Forkhead box M1 (FoxM1) transcription factor plays crucial roles in multiple biological processes, including cell proliferation, differentiation, migration, and transformation. Recent studies have reported that aberrant expression of FoxM1 was found in a variety of human cancers. However, the expression pattern of FoxM1 and its clinical significance in human hepatocellular carcinoma (HCC) have not been well characterized to date. In this study, the expression of FoxM1 was evaluated in 46 pairs of human HCC, the adjacent non-tumorous liver tissues, and 12 pairs of normal liver tissues by immumohistochemistry. FoxM1 expression was upregulated in the HCC (76.09 %) compared with non-tumorous liver tissues (39.13 %) and normal liver tissues (8.33 %) (P < 0.05). FoxM1 expression was significantly associated with tumor stage, tumor size, tumor number, integrality of tumor encapsulation, tumor thrombus, and AFP level (P < 0.05). Functionally, enforced expression of FoxM1 in HCC cell line (HHCC) remarkably enhanced cell proliferation in vitro and in vivo. Further analysis of cell cycle-related molecules showed that FoxM1 overexpression increased expressions of cyclin B1 and cyclin D1 but reduced expressions of p27(Kip1) and p21(Cip1). Our findings suggest that FoxM1 overexpression promotes HCC cell proliferation by cell cycle regulation, which is a potential target for hepatocellular carcinoma therapy.

Purpose: Lamina-associated polypeptide 2 (LAP2; encoded by TMPO ), is a nuclear protein that may affect chromatin regulation and gene expression through dynamically binding to nuclear lamin. TMPO (LAP2) plays dual roles of either suppressing or promoting proliferation of cells, depending on the status of the cell. It has been reported that TMPO is up-regulated in various cancer types. However, its function in lung cancer has not been studied yet. Materials and methods: A series of clinical microarray datasets for lung cancer were investigated to demonstrate the expression of TMPO. The transcription of TMPO gene in human lung cancer was analyzed using Oncomine platform (www.oncomine.org) according to the standardized procedures described previously. Four separate datasets (Hou Lung, Okayama Lung, Beer Lung, and Garber Lung) were analyzed. Results: Here, we show that TMPO is over-expressed in lung cancer tissues, and that a high level of TMPO indicates a poor prognosis in lung cancer patients. Knockdown of TMPO in lung cancer cells inhibits cell proliferation and induces apoptosis. Also, down-regulation of TMPO leads to an impaired metastatic ability of tumor cells. A nude mice tumor model show that knockdown of TMPO suppresses tumor formation in vivo. Conclusion: Collectively, this study suggests TMPO as an oncogene and a novel prognostic gene in lung cancer.

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