Key result
RELN overexpression impairs TGF-β1-driven hepatocellular carcinoma cell migration.
Why the study?
Reducing HCC-associated metastasis depends on uncovering molecular signaling pathways that promote HCC metastasis.
TGF-β1 promotes hepatocellular carcinoma cell migration by suppressing the expression of RELN, identifying a potential molecular pathway involved in HCC metastasis.
Answers are grounded in this paper and cite their sources.
Suggests RELN as a potential brake on HCC migration; leaves open translation to human metastasis models.
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.
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Luo et al. (2018) studied Hepatocellular carcinoma. TGF-β1 and RELN expression modulation was evaluated on Cell migration ability. TGF-β1 enhanced hepatocellular carcinoma cell migration by repressing RELN expression, whereas overexpression of RELN impaired TGF-β1-enhanced cell migration.
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