Long non-coding RNA ASMTL-AS1 deteriorates the oncogenicity of osteosarcoma by decoying microRNA-342-3p and consequently raising ADAM9 expression.

Szczegóły
Abstrakt

Tytuł:: Long non-coding RNA ASMTL-AS1 deteriorates the oncogenicity of osteosarcoma by decoying microRNA-342-3p and consequently raising ADAM9 expression.
Autorzy:: Hou C; Department of Hand, Foot and Ankle Surgery, Zaozhuang Municipal Hospital, Shandong, 277100, China.
Sun F; Medical College, Zaozhuang Vocational College, Shandong, 277800, China.
Sun M; Department of Traumatic Orthopedics, Zaozhuang Municipal Hospital, Shandong, 277100, China. Electronic address: mingyue5921_.
Źródło:: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2021 Nov 19; Vol. 579, pp. 89-96. Date of Electronic Publication: 2021 Sep 22.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Publication: <2002- >: San Diego, CA : Elsevier
Original Publication: New York, Academic Press.
MeSH Terms:: Gene Expression Regulation, Neoplastic*
ADAM Proteins/*biosynthesis
Membrane Proteins/*biosynthesis
Methyltransferases/*genetics
Osteosarcoma/*metabolism
RNA, Antisense/*genetics
RNA, Long Noncoding/*genetics
ADAM Proteins/genetics ; Animals ; Antineoplastic Agents/pharmacology ; Apoptosis ; Carcinogenesis ; Cell Line, Tumor ; Cell Proliferation ; Gene Expression Profiling ; Gene Expression Regulation ; Gene Silencing ; Humans ; In Vitro Techniques ; Male ; Membrane Proteins/genetics ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNAs/genetics ; Neoplasm Transplantation ; Osteoblasts/metabolism ; Osteosarcoma/genetics ; RNA, Small Interfering/metabolism
Contributed Indexing:: Keywords: Long non-coding RNA; OS therapy; SMTL antisense RNA 1; Therapeutic target
Substance Nomenclature:: 0 (Antineoplastic Agents)
0 (MIRN342 microRNA, human)
0 (Membrane Proteins)
0 (MicroRNAs)
0 (RNA, Antisense)
0 (RNA, Long Noncoding)
0 (RNA, Small Interfering)
EC 2.1.1.- (ASMTL protein, human)
EC 2.1.1.- (Methyltransferases)
EC 3.4.24.- (ADAM Proteins)
EC 3.4.24.- (ADAM9 protein, human)
Entry Date(s):: Date Created: 20211001 Date Completed: 20211227 Latest Revision: 20211227
Update Code:: 20240105
DOI:: 10.1016/j.bbrc.2021.09.049
PMID:: 34597997
: Czasopismo naukowe

Full Text Finder

Background: Till now, little is known regarding expression pattern and specific roles of lncRNA ASMTL antisense RNA 1 (ASMTL-AS1) in osteosarcoma (OS). Therefore, our current research measured the expression of ASMTL-AS1 in OS, unveiled the roles of ASMTL-AS1 in the modulation of malignant characteristics of OS, and identified the downstream mechanism.
Methods: The regulatory actions of ASMTL-AS1 ablation in OS cells were explored utilizing loss-of-function experiments. Mechanistic studies were implemented utilizing bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation and rescue experiments.
Results: ASMTL-AS1 expression in OS was elevated in both TCGA database and our own cohort. Interfering with ASMTL-AS1 restricted cell proliferation, migration and invasion while increasing cell apoptosis in vitro. Additionally, silencing ASMTL-AS1 blocked tumour growth in vivo. Mechanistically, ASMTL-AS1 could act as a competing endogenous RNA for microRNA-342-3p (miR-342-3p) and inhibit its activity in OS cells, consequently causing an increase in ADAM metallopeptidase domain 9 (ADAM9) levels. Furthermore, inhibiting miR-342-3p or upregulating ADAM9 abated silenced ASMTL-AS1-induced antitumour activity in OS cells.
Conclusion: ASMTL-AS1 aggravated OS progression by regulating the miR-342-3p/ADAM9 axis.
Competing Interests: Declaration of competing interest The authors declare that they have no competing interests.
(Copyright © 2021 Elsevier Inc. All rights reserved.)

Informacja