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肌动蛋白样蛋白6A预示肝细胞癌预后不良，并促进转移和上皮-间质转化。

Actin-like 6A predicts poor prognosis of hepatocellular carcinoma and promotes metastasis and epithelial-mesenchymal transition.

作者信息

Xiao Shuai, Chang Rui-Min, Yang Ming-Yang, Lei Xiong, Liu Xiao, Gao Wen-Bin, Xiao Jing-Lei, Yang Lian-Yue

机构信息

Liver Cancer Laboratory, Department of Surgery, Xiangya Hospital, Central South University, Changsha, China.

出版信息

Hepatology. 2016 Apr;63(4):1256-71. doi: 10.1002/hep.28417. Epub 2016 Jan 26.

DOI:10.1002/hep.28417
PMID:26698646
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4834727/
Abstract

UNLABELLED

Hepatocellular carcinoma (HCC) is one of the most lethal cancers worldwide because of metastasis. Epithelial-mesenchymal transition (EMT) is widely considered to be crucial to the invasion-metastasis cascade during cancer progression. Actin-like 6A (ACTL6A) is initially verified important for cell proliferation, differentiation, and migration. In this study, we find that ACTL6A plays an essential role in metastasis and EMT of HCC. ACTL6A expression is up-regulated in HCC cells and tissues. A high level of ACTL6A in HCCs is correlated with aggressive clinicopathological features and is an independent poor prognostic factor for overall and disease-free survival of HCC patients. Ectopic expression of ACTL6A markedly promotes HCC cells migration, invasion, as well as EMT in vitro and promotes tumor growth and metastasis in the mouse xenograft model. Opposite results are observed when ACTL6A is knocked down. Mechanistically, ACTL6A promotes metastasis and EMT through activating Notch signaling. ACTL6A knockdown has the equal blockage effect as the Notch signaling inhibitor, N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butylester, in HCC cells. Further studies indicate that ACTL6A might manipulate SRY (sex determining region Y)-box 2 (SOX2) expression and then activate Notch1 signaling.

CONCLUSIONS

ACTL6A promotes metastasis and EMT by SOX2/Notch1 signaling, indicating a prognostic biomarker candidate and a potential therapeutic target for HCC.

摘要

未标记

肝细胞癌（HCC）是全球最致命的癌症之一，原因在于其会发生转移。上皮-间质转化（EMT）被广泛认为在癌症进展过程中的侵袭-转移级联反应中至关重要。肌动蛋白样6A（ACTL6A）最初被证实对细胞增殖、分化和迁移很重要。在本研究中，我们发现ACTL6A在HCC的转移和EMT中起关键作用。ACTL6A在HCC细胞和组织中表达上调。HCC中高水平的ACTL6A与侵袭性临床病理特征相关，并且是HCC患者总体生存和无病生存的独立不良预后因素。ACTL6A的异位表达在体外显著促进HCC细胞迁移、侵袭以及EMT，并在小鼠异种移植模型中促进肿瘤生长和转移。当ACTL6A被敲低时，观察到相反的结果。机制上，ACTL6A通过激活Notch信号促进转移和EMT。在HCC细胞中，敲低ACTL6A具有与Notch信号抑制剂N-[N-(3,5-二氟苯乙酰基)-L-丙氨酰基]-S-苯甘氨酸叔丁酯相同的阻断作用。进一步研究表明，ACTL6A可能调控性别决定区Y框蛋白2（SOX2）的表达，进而激活Notch1信号。

结论

ACTL6A通过SOX2/Notch1信号促进转移和EMT，表明其是HCC的一个预后生物标志物候选物和潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e8/4834727/8d702e9d142d/HEP-63-1256-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e8/4834727/ea057848f782/HEP-63-1256-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e8/4834727/63b582bbbd28/HEP-63-1256-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e8/4834727/68ea2c2b813f/HEP-63-1256-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e8/4834727/0323ff56efc3/HEP-63-1256-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e8/4834727/fcb7fda3b6ca/HEP-63-1256-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e8/4834727/8d702e9d142d/HEP-63-1256-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e8/4834727/ea057848f782/HEP-63-1256-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e8/4834727/63b582bbbd28/HEP-63-1256-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e8/4834727/68ea2c2b813f/HEP-63-1256-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e8/4834727/0323ff56efc3/HEP-63-1256-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e8/4834727/fcb7fda3b6ca/HEP-63-1256-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4e8/4834727/8d702e9d142d/HEP-63-1256-g006.jpg

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