Oncotarget

Research Papers:

miR-1236 down-regulates alpha-fetoprotein, thus causing PTEN accumulation, which inhibits the PI3K/Akt pathway and malignant phenotype in hepatoma cells

Rui Gao, Chunli Cai, Jiancheng Gan, Xi Yang, Zeyu Shuang, Min Liu, Shengping Li and Hua Tang _

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Oncotarget. 2015; 6:6014-6028. https://doi.org/10.18632/oncotarget.3338

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Abstract

Rui Gao1,*, Chunli Cai1,*, Jiancheng Gan2,*, Xi Yang1, Zeyu Shuang3, Min Liu1, Shengping Li3 and Hua Tang1

1 Tianjin Life Science Research Center and Basic Medical School, Tianjin Medical University, Tianjin, China

2 Department of Surgery, Secondary Hospital of Tianjin Medical University, Tianjin, China

3 State Key Laboratory of Oncology in Southern China, Department of Hepatobiliary Oncology, Cancer Center, Sun Yat-sen University, Guangzhou, China

* These authors contributed equally to this work

Correspondence to:

Hua Tang, email:

Shengping Li, email:

Keywords: microRNA; microRNA-1236; AFP; PTEN; hepatocellular cancer

Received: November 09, 2014 Accepted: January 14, 2015 Published: January 21, 2015

Abstract

Alpha fetoprotein (AFP) is a clinical biomarker of hepatocellular carcinoma (HCC). Here, we found that miR-1236 is down-regulated, whereas AFP is highly expressed in HCC tissues and cells. We demonstrated that miR-1236 directly targets the 3’UTR of AFP and down-regulates its expression. Also, miR-1236 inhibited and AFP stimulated proliferation, migration, invasion and vasculogenic mimicry (VM) of HCC. In agreement, AFP over-expression counteracted the inhibitory effect of miR-1236. We demonstrated that AFP promoted the ubiquitination of PTEN, thus decreasing PTEN levels, while miR-1236 inhibited the PI3K/Akt pathway.


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