Background & Aims: Given the pivotal role of Zfp36l1b in angiogenesis, proliferation and migration of endothelial cells, we aimed to explore its role in HCC metastasis. Methods: Zfp36l1b expressions in HCC tissues and cells were assessed by qRT-PCR, western blot and immunohistochemistry. The effect of Zfp36l1b on HCC metastasis was studied in vitro and in vivo . Results: Zfp36l1b was frequently down-regulated in HCC and its expression level was significantly associated with aggressive clinicopathological features and overall and disease-free survival of HCC patients after hepatectomy. Loss of Zfp36l1b markedly promoted HCC cells invasion and migration in vitro , and facilitated tumor metastasis in vivo . Conclusions: Zfp36l1b contributes to the development and progression of HCC as an anti-oncogene and may serve as a valuable prognostic marker for HCC patients.
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Chen et al. (2024) studied this question.
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