Abstract
Zinc-fingers and homeoboxes 1 (ZHX1) is a transcription repressor that has been associated with the progressions of hepatocellular carcinoma, gastric cancer, and breast cancer. However, the functional roles of ZHX1 in cholangiocarcinoma (CCA) have not been determined. We investigated the expression and roles of ZHX1 during the proliferation, migration, and invasion of CCA cells. In silico analysis and immunohistochemical studies showed amplification and overexpression of ZHX1 in CCA tissues. Furthermore, ZHX1 knockdown using specific siRNAs decreased CCA cell proliferation, migration, and invasion, whereas ZHX1 overexpression promoted all three characteristics. In addition, results suggested EGR1 might partially mediate the effect of ZHX1 on the proliferation of CCA cells. Taken together, these results show ZHX1 promotes CCA cell proliferation, migration, and invasion, and present ZHX1 as a potential target for the treatment of CCA.
Highlights
Cholangiocarcinoma (CCA) is a malignant tumor arising from biliary epithelial cells, and is the sixth leading cause of gastrointestinal cancer in the West and presents a high incidence rate in East Asia [1, 2]
To further confirm whether Zinc-fingers and homeoboxes 1 (ZHX1) is overexpressed in CCA, we examined the expressional status of ZHX1 in patients’ CCA tissues using immunohistochemistry, which was performed on 4-μm paraffin-embedded sections
All results for effects of ZHX1 on cholangiocarcinoma cells were summarized as a table (S1 Table)
Summary
Cholangiocarcinoma (CCA) is a malignant tumor arising from biliary epithelial cells, and is the sixth leading cause of gastrointestinal cancer in the West and presents a high incidence rate in East Asia [1, 2]. Clinical features of the disease are determined by location and clinical stage. Clinical staging which is essential for treatment and prognosis [5], depends on size, lymph node invasion, and metastasis to other tissues. No specific symptoms are observed during early stage disease and no specific early stage markers have been identified [6], and CCA is usually detected in the late stage. In common with some other cancers, late detection limits the likelihood of complete tumor resection, and compromises the effectiveness of therapeutic treatments because cancer cells have already invaded lymph nodes and other tissues [7]. The identification of molecular targets related to the migration and invasion of CCA is of considerable therapeutic and prognostic importance
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