Research Papers:

This article has been retracted. Retraction in: Oncotarget. 2022; 13:1201-1201.

SAMMSON drives the self-renewal of liver tumor initiating cells through EZH2-dependent Wnt/β-catenin activation

Xiaopeng Li, Ming Li, JiaLi Chen, Hua Dai, Liang Wang, Ying Xiong, Yuanbin Zhong and Lunli Zhang _

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Oncotarget. 2017; 8:103785-103796. https://doi.org/10.18632/oncotarget.21792

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Xiaopeng Li1,*, Ming Li1,*, JiaLi Chen2, Hua Dai3, Liang Wang1, Ying Xiong1, Yuanbin Zhong1 and Lunli Zhang1

1Department of Infectious Disease, The First Affiliated Hospital of Nanchang University, Nanchang, JiangXi 330006, China

2Department of Function, JiangXi Children’s Hospital, Nanchang, JiangXi 330006, China

3Department of Pathology, The First Affiliated Hospital of Nanchang University, Nanchang, JiangXi 330006, China

*These authors have contributed equally to this work

Correspondence to:

Lunli Zhang, email: [email protected]

Keywords: liver TICs, SAMMSON, EZH2, Wnt/β-catenin, self-renewal

Received: August 25, 2017     Accepted: September 24, 2017     Published: October 10, 2017


Liver cancer is one of the most serious cancers all over the world. Liver tumor initiating cells (TICs) account for tumor initiation and metastasis. However, the regulatory mechanism of liver TICs remains unclear. Here we found long noncoding RNA SAMMSON is highly expressed in liver cancer and liver TICs. SAMMSON silenced cells show impaired self-renewal capacity, while, its overexpression induces enhanced self-renewal. SAMMSON drives the activation of Wnt/β-catenin signaling, and thus promotes liver TIC self-renewal. SAMMSON interacts with EZH2, a core component of PRC2 complex, and inhibits the expression of CTNNBIP1 through EZH2 dependent manner. SAMMSON binds to CTNNBIP1 promoter and recruits EZH2 to CTNNBIP1 promoter. What’s more, targeting liver TICs through SAMMSON, EZH2 and Wnt/β-catenin signaling impaired liver TIC self-renewal, decreased tumor propagation and severity. Taken together, SAMMSON drives liver TIC self-renewal through EZH2-dependent Wnt/β-catenin activation.

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