| Objective:To explore the expression of transcription factor Sp1/KLF6, determine the regulation of Sp1/KLF6on tumor metastasis related gene basigin-2and observe roles of KLF6on hepatocellular carcinoma cells invasion and metastasis. Methods: Hepatocellular carcinoma cells and normal hepatocytes were cultured. In purified total RNA and lysis protein, expression levels of Sp1, KLF6and basigin-2were detected using realtime RT-PCR and western blot. Then the binding of KLF6with basigin-2promoter and Sp1promoter genome DNA were detected by chromatin immunoprecipitation (ChIP) and the transcriptional regulation of KLF6on basigin-2and Sp1were inspected with luciferase reporter assay system. Through overexpressing or interfering KLF6, the expression regulation of KLF6on Sp1and basigin-2were observed, and the role of KLF6on hepatocellular carcinoma cells invasion was explored using in vitro transwell invasion assay. Results:Compared to normal hepatocyte control, the expression levels of Sp1and basigin-2were obviously up-regulated both in mRNA level and protein level, however those of KLF6were down-regulated. Transcription factor KLF6could bind to genome DNA located on the promoter region of basigin-2and Sp1, inhibit Sp1mediated transcriptional activation and repress basigin-2transcription. Overexpressing KLF6in HCC cells could inhibit the expression of Sp1and basigin-2, while koncking down KLF6could upregulate the expression of Sp1and basigin-2. Overexpressed KLF6also could inhibit hepatocellular carcinoma cells invasion and metastasis. Conclusion:Transcription factor Sp1/KLF6invovled in the transcriptional regulation of basigin-2. Sp1acted as transcription activator while KLF6as repressor, the interaction of Sp1and KLF6controlled the expression of basigin-2. KLF6could inhibit basigin-2mediated hepatocellular carcinoma cells invasion and metastasis. |
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