Elevated FOXA1 Expression Indicates Poor Prognosis in Liver Cancer due to Its Effects on Cell Proliferation and
Zhenrong Liu1, Yaru Wang1, Zulihumaer Aizimuaji1
1State Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
Purpose:
Studying the pathogenesis of liver cancer is conducive to the exploration of effective diagnostic and prognostic biomarkers. In this study, we investigated the expression of FOXA1 and its oncogenic role in hepatocellular carcinoma (HCC).
Methods:
Transcriptome data of HCC tissues were downloaded from The Cancer Genome Atlas (TCGA) and GEO databases and analyzed using R software. We also upregulated FOXA1 expression in HCC cells and investigated the role of FOXA1 in the proliferation and migration of HCC cells through proliferation, colony formation, wound healing, and Transwell assays.
Results:
An analysis of the transcriptome data in TCGA database revealed found that FOXA1 is highly expressed in HCC tissues and that patients with low FOXA1 expression have a better prognosis. High FOXA1 expression was mainly associated with extracellular matrix organization, cancer, and mitosis. The results of an immunohistochemistry (IHC) assay showed that FOXA1 protein was highly expressed in HCC tissues, and patients with low FOXA1 expression showed longer disease-specific survival times and progression-free intervals. The results from quantitative reverse transcription-PCR (RT-qPCR) and Western blot experiments showed that the expression of FOXA1 in liver cancer cell lines was higher than that in immortalized human liver cell lines. Proliferation, wound healing, and Transwell experiments showed that FOXA1 enhanced the proliferation and migration abilities of liver cancer and immortalized human cell lines.
Conclusion:
Our research suggests that FOXA1 plays an important role in promoting the recurrence and metastasis of HCC by increasing cell proliferation and metastasis.
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