UHRF1 suppression promotes cell differentiation and reduces inflammatory reaction in anaplastic thyroid cancer
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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
Quentin Liu, email: email@example.com
Zi-Jie Long, email: firstname.lastname@example.org
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
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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