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TRIM29 通过抑制 Wnt/β-catenin 信号通路来阻止肝细胞癌的进展。

TRIM29 prevents hepatocellular carcinoma progression by inhibiting Wnt/β-catenin signaling pathway.

机构信息

Department of Hepatobiliary Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.

出版信息

Acta Biochim Biophys Sin (Shanghai). 2019 Jan 1;51(1):68-77. doi: 10.1093/abbs/gmy151.

Abstract

TRIM29 plays an important role in many neoplasms. In this study, we aimed to elucidate its role in hepatocellular carcinoma (HCC) and explore the corresponding potential mechanism. The expression level of TRIM29 in HCC samples and hepatoma cell lines was detected. We found that TRIM29 was down-regulated in clinical HCC samples and cultured hepatoma cell lines by western blot analysis and quantitative polymerase chain reaction. In addition, we demonstrated that higher TRIM29 expression was associated with higher differentiation grade of HCC. To explore the effect of TRIM29 on hepatoma cells and its possible mechanisms, TRIM29-knockdown and overexpression cell models were constructed. The results showed that the depletion of TRIM29 promoted liver cancer cell proliferation, clone formation, migration and invasion in vitro probably through the Wnt/β-catenin signaling pathway. This study revealed the inhibitory roles of TRIM29 in HCC and the possible mechanisms.

摘要

TRIM29 在许多肿瘤中发挥着重要作用。在本研究中,我们旨在阐明其在肝细胞癌(HCC)中的作用,并探讨相应的潜在机制。检测了 TRIM29 在 HCC 样本和肝癌细胞系中的表达水平。通过 Western blot 分析和定量聚合酶链反应,我们发现 TRIM29 在临床 HCC 样本和培养的肝癌细胞系中下调。此外,我们证明,TRIM29 的高表达与 HCC 的高分化程度有关。为了探讨 TRIM29 对肝癌细胞的影响及其可能的机制,构建了 TRIM29 敲低和过表达细胞模型。结果表明,TRIM29 的耗竭促进了肝癌细胞在体外的增殖、克隆形成、迁移和侵袭,可能是通过 Wnt/β-catenin 信号通路。本研究揭示了 TRIM29 在 HCC 中的抑制作用及其可能的机制。

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