TGF-β1 promotes cell migration in hepatocellular carcinoma by suppressing reelin expression
Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer in adults and is a leading cause of worldwide cancer mortality. Intrahepatic dissemination and extrahepatic metastasis are key factors in malignant growth of HCC. Reducing HCC-associated metastasis is critically dependent...
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Published in | Gene Vol. 688; pp. 19 - 25 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Netherlands
Elsevier B.V
10.03.2019
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Subjects | |
Online Access | Get full text |
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Summary: | Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer in adults and is a leading cause of worldwide cancer mortality. Intrahepatic dissemination and extrahepatic metastasis are key factors in malignant growth of HCC. Reducing HCC-associated metastasis is critically dependent on uncovering molecular signaling pathways that promote HCC metastasis. In this study, we explored the effect of TGF-β1 and RELN on cell migration, and the relationship between TGF-β1 and RELN in HCC cells. The data presented that TGF-β1 and RELN showed an opposite expression pattern, and either increased expression of TGF-β1 or decreased expression of RELN increased HCC cell migration ability. We also found TGF-β1 enhanced cell migration ability was through repressing RELN expression, as overexpression of RELN impaired TGF-β1 enhanced cell migration. Our work revealed the relationship between TGF-β1 and RELN and uncovered the important role of RELN in suppressing cell migration in HCC cells.
•This study profiled the expression of TGF-β1 and RELN in normal liver cell and HCC cells, and found these two genes present an opposite expression pattern.•TGF-β1 functions upstream of RELN and suppresses the expression of RELN, which leads to increased HCC cell migration ability.•This study provides new insights into the development of novel treatment options preventing HCC cell metastasis and improving patients’ survival. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0378-1119 1879-0038 |
DOI: | 10.1016/j.gene.2018.11.033 |