LINC00266-1/miR-548c-3p/SMAD2 feedback loop stimulates the development of osteosarcoma.


Journal

Cell death & disease
ISSN: 2041-4889
Titre abrégé: Cell Death Dis
Pays: England
ID NLM: 101524092

Informations de publication

Date de publication:
24 07 2020
Historique:
received: 26 11 2019
accepted: 09 07 2020
revised: 04 07 2020
entrez: 26 7 2020
pubmed: 28 7 2020
medline: 27 3 2021
Statut: epublish

Résumé

Osteosarcoma (OS) is one of the most common primary bone malignancies and accounts for 3.4% of pediatric tumors. Its 5-year survival is as low as about 20%. Differentially expressed lncRNAs in OS profiling were searched in the downloaded profile of GSE12865. As a result, LINC00266-1 was detected to be upregulated in both GSE12865 and OS tissues we collected. SMAD2 was the downstream target binding to promoter sites of LINC00266-1, displaying a positive regulatory interaction. Knockdown of LINC00266-1 suppressed the proliferative and metastatic abilities, and promoted the apoptosis in OS cells. Besides, knockdown of LINC00266-1 significantly alleviated the growth of OS in vivo. MiR-548c-3p was the sponge miRNA of LINC00266-1, which was able to reverse the regulatory effects of LINC00266-1 on OS cell phenotypes. Moreover, miR-548c-3p bound to the 3'-UTR of SMAD2 and thus downregulated SMAD2. Overexpression of SMAD2 partially reversed the regulatory effects of LINC00266-1 on OS cell phenotypes. Finally, we have identified that LINC00266-1/miR-548c-3p/SMAD2 feedback loop was responsible for stimulating the development of OS.

Identifiants

pubmed: 32709857
doi: 10.1038/s41419-020-02764-8
pii: 10.1038/s41419-020-02764-8
pmc: PMC7381647
doi:

Substances chimiques

MIRN548 microRNA, human 0
MicroRNAs 0
RNA, Long Noncoding 0
SMAD2 protein, human 0
Smad2 Protein 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

576

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Auteurs

Shengnai Zheng (S)

Department of Orthopedic Surgery, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China.

Li Wan (L)

Department of Oncology, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, 223300, Huai'an, Jiangsu, China.

Dawei Ge (D)

Department of Orthopedic Surgery, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China.

Fan Jiang (F)

Department of Orthopedics, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, Jiangsu, China.

Zhanyang Qian (Z)

Department of Orthopedics, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, Jiangsu, China.

Jian Tang (J)

Burn and Plastic Surgery, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, Jiangsu, China.

Jin Yang (J)

Department of Pathology, Wuxi Third People's Hospital, 214000, Wuxi City, Jiangsu, China.

Yilun Yao (Y)

Department of Orthopedic Surgery, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China.

Junwei Yan (J)

Department of Orthopedic Surgery, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China.

Lei Zhao (L)

Department of Orthopedic Surgery, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China.

Haijun Li (H)

Department of Orthopedics, Taizhou People's Hospital Affiliated to Nantong University, 225300, Taizhou, Jiangsu, China.

Lei Yang (L)

Department of Orthopedic Surgery, Nanjing First Hospital, Nanjing Medical University, 210006, Nanjing, Jiangsu, China. leiyang@njmu.edu.cn.

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