Oncotarget

Research Papers:

UHRF1 suppression promotes cell differentiation and reduces inflammatory reaction in anaplastic thyroid cancer

Bi-Cheng Wang _, Guo-He Lin, Bo Wang, Min Yan, Bin He, Wei Zhang, An-Kui Yang, Zi-Jie Long and Quentin Liu

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Oncotarget. 2018; 9:31945-31957. https://doi.org/10.18632/oncotarget.10674

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Abstract

Bi-Cheng Wang1,*, Guo-He Lin1,*, Bo Wang2,*, Min Yan1, Bin He1, Wei Zhang1, An-Kui Yang1, Zi-Jie Long3,4, Quentin Liu1,3,4,5

1State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, Guangzhou, 510060, China

2Department of Medical Oncology, The Eastern Hospital of The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510700, China

3Department of Hematology, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510630, China

4Institute of Hematology, Sun Yat-sen University, Guangzhou, 510630, China

5Institute of Cancer Stem Cell, Dalian Medical University, Dalian, 116044, China

*These authors have contributed equally to this work

Correspondence to:

Quentin Liu, email: liuq9@mail.sysu.edu.cn

Zi-Jie Long, email: longzij@mail.sysu.edu.cn

Keywords: UHRF1, anaplastic thyroid cancer, proliferation, differentiation, inflammatory reaction

Received: January 09, 2016    Accepted: June 02, 2016    Epub: July 18, 2016    Published: August 10, 2018

ABSTRACT

Anaplastic thyroid cancer (ATC), an undifferentiated subtype of thyroid cancer, is one of the most malignant endocrine cancer with low survival rate, and resistant to chemotherapy and radiation therapy. Here we found that UHRF1 was highly expressed in human ATC compared with normal tissue and papillary thyroid cancer (PTC). Knockdown of UHRF1 inhibited proliferation of ATC in vitro and in vivo. Consistently, overexpression of UHRF1 promoted the proliferation of thyroid cancer cells. Moreover, UHRF1 suppression induced differentiation of three-dimensional (3D) cultured ATC cells and down-regulated the expression of dedifferentiation marker (CD97). The stem cell markers (Sox2, Oct4 and Nanog) were suppressed simultaneously. In addition, UHRF1 knockdown reduced the transcription of cytokines (IL-8, TGF-α and TNF-α), which might relieve the inflammatory reaction in ATC patients. This study demonstrated a role of UHRF1 in ATC proliferation, dedifferentiation and inflammatory reaction, presenting UHRF1 as a potential target in ATC therapy.


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