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微小RNA-98通过靶向SALL4在肝细胞癌中发挥肿瘤抑制作用。

MicroRNA-98 acts as a tumor suppressor in hepatocellular carcinoma via targeting SALL4.

作者信息

Zhou Wuyuan, Zou Benkui, Liu Lisheng, Cui Kai, Gao Jie, Yuan Shuanghu, Cong Ning

机构信息

Department of Hepatobillary Surgery, Shandong Cancer Hospital, Jinan, Shandong 250117, P.R. China.

Department of Urology Surgery, Shandong Cancer Hospital, Jinan, Shandong 250117, P.R. China.

出版信息

Oncotarget. 2016 Nov 8;7(45):74059-74073. doi: 10.18632/oncotarget.12190.

DOI:10.18632/oncotarget.12190
PMID:27677076
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5342035/
Abstract

MicroRNAs (miRs) are involved in the development and progression of hepatocellular carcinoma (HCC), but the regulatory mechanism of miR-98 in HCC still remains unclear. Here we found that miR-98 was significantly downregulated in HCC tissues compared to matched adjacent normal tissues (ANTs). Low miR-98 expression was associated with tumor size, metastasis, portal vein tumor embolus, and poor overall survival. Ectopic expression of miR-98 decreased the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of HCC cells. SALL4 was identified as a novel target of miR-98, and the protein expression of SALL4 was inhibited by miR-98 in HCC cells. Overexpression of SALL4 reversed the suppressive effects of miR-98 on the malignant phenotypes of HCC cells. Besides, SALL4, upregulated in HCC tissues compared to the matched ANTs, was inversely correlated to the miR-98 levels in HCC tissues. In addition, overexpression of miR-98 markedly suppressed the tumor growth as well as tumor-induced death in nude mice. In summary, miR-98 plays a suppressive role in the proliferation, migration, invasion and EMT of HCC cells, partly at least, via directly inhibition of SALL4. Therefore, the miR-98/SALL4 axis may become a promising therapeutic target for HCC.

摘要

微小RNA（miR）参与肝细胞癌（HCC）的发生和发展，但miR-98在HCC中的调控机制仍不清楚。在此我们发现，与配对的癌旁正常组织（ANT）相比，miR-98在HCC组织中显著下调。低miR-98表达与肿瘤大小、转移、门静脉癌栓及较差的总生存期相关。miR-98的异位表达降低了HCC细胞的增殖、迁移、侵袭及上皮-间质转化（EMT）。SALL4被鉴定为miR-98的一个新靶点，miR-98在HCC细胞中抑制SALL4的蛋白表达。SALL4的过表达逆转了miR-98对HCC细胞恶性表型的抑制作用。此外，与配对的ANT相比，SALL4在HCC组织中上调，且与HCC组织中的miR-98水平呈负相关。另外，miR-98的过表达显著抑制了裸鼠的肿瘤生长及肿瘤诱导的死亡。总之，miR-98至少部分通过直接抑制SALL4在HCC细胞的增殖、迁移、侵袭及EMT中发挥抑制作用。因此，miR-98/SALL4轴可能成为HCC一个有前景的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/58c7cc10daca/oncotarget-07-74059-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/914ef8ad31f8/oncotarget-07-74059-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/912ac62b57e7/oncotarget-07-74059-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/d4f3f1959a35/oncotarget-07-74059-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/abfc7b8131a3/oncotarget-07-74059-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/23ad82589a29/oncotarget-07-74059-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/200389c31fb3/oncotarget-07-74059-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/48862266f8d9/oncotarget-07-74059-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/7bac67232084/oncotarget-07-74059-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/07ee99330eff/oncotarget-07-74059-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/58c7cc10daca/oncotarget-07-74059-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/914ef8ad31f8/oncotarget-07-74059-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/912ac62b57e7/oncotarget-07-74059-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/d4f3f1959a35/oncotarget-07-74059-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/abfc7b8131a3/oncotarget-07-74059-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/23ad82589a29/oncotarget-07-74059-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/200389c31fb3/oncotarget-07-74059-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/48862266f8d9/oncotarget-07-74059-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/7bac67232084/oncotarget-07-74059-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/07ee99330eff/oncotarget-07-74059-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d2b/5342035/58c7cc10daca/oncotarget-07-74059-g010.jpg

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