Long non-coding HOXA-AS3 contributes to osteosarcoma progression through the miR-1286/TEAD1 axis

Long non-coding RNA (lncRNA) HOXA cluster antisense RNA 3 (HOXA-AS3) regulates the progression of several types of human malignancy. However, the role and potential mechanism of HOXA-AS3 in osteosarcoma (OS) remain unknown. In this study, upregulation of HOXA-AS3 was observed in OS tissues and cell...

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Published in:Journal of orthopaedic surgery and research Vol. 18; no. 1; pp. 730 - 14
Main Authors: Xiao, Xiangjun, Liu, Mingjiang, Xie, Songlin, Liu, Changxiong, Huang, Xinfeng, Huang, Xiongjie
Format: Journal Article
Language:English
Published: London BioMed Central 27.09.2023
BioMed Central Ltd
Springer Nature B.V
BMC
Subjects:
Antibodies
Antisense RNA
B cells
Biotechnology
Bone cancer
Bone Neoplasms - genetics
Cell growth
Cell Line, Tumor
Cell lines
Cell proliferation
Cell Proliferation - genetics
Chemotherapy
Development and progression
Endothelial cells
Endothelial Cells - metabolism
Ewings sarcoma
Gene Expression Regulation, Neoplastic - genetics
Health aspects
HOXA cluster antisense RNA 3
Humans
Malignancy
Medical prognosis
Medicine
Medicine & Public Health
Metastasis
MicroRNAs - genetics
MicroRNAs - metabolism
MiR-1286
Orthopedics
Osteosarcoma
Osteosarcoma - genetics
Osteosarcoma - pathology
Polymerase chain reaction
Proteins
Radiation therapy
Reagents
Research Article
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Sarcoma
Software
Statistical analysis
Stem cells
Surgical Orthopedics
TEA domain family mem
TEA Domain Transcription Factors - genetics
TEA Domain Transcription Factors - metabolism
Therapeutic targets
Tumorigenesis
Tumors
Umbilical vein
China
United States > US
MiR-1286
Osteosarcoma
HOXA cluster antisense RNA 3
TEA domain family mem
ISSN:1749-799X, 1749-799X
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Summary:Long non-coding RNA (lncRNA) HOXA cluster antisense RNA 3 (HOXA-AS3) regulates the progression of several types of human malignancy. However, the role and potential mechanism of HOXA-AS3 in osteosarcoma (OS) remain unknown. In this study, upregulation of HOXA-AS3 was observed in OS tissues and cell lines and associated with poor clinical outcomes. Silencing of HOXA-AS3 significantly inhibited the proliferation, migration and invasion of OS cells in vitro and suppressed the tumorigenesis of OS cells in vivo. Furthermore, knockdown of HOXA-AS3 inhibited the proliferation and migration of human umbilical vein endothelial cells (HUVECs) and epithelial-to-mesenchymal transition (EMT) in OS. Further investigation of this mechanism revealed that HOXA-AS3 could directly upregulate the expression of TEAD1 via its competing endogenous RNA (ceRNA) activity on miR-1286. This study clarified the oncogenic roles of the HOXA-AS3/miR-1286/TEAD1 axis in OS progression, suggesting a novel therapeutic target for OS.
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ISSN:1749-799X
1749-799X
DOI:10.1186/s13018-023-04214-5