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Long non-coding RNA ASMTL-AS1 deteriorates the oncogenicity of osteosarcoma by decoying microRNA-342-3p and

Chengcai Hou1, Fei Sun2, Mingyue Sun3

  • 1Department of Hand, Foot and Ankle Surgery, Zaozhuang Municipal Hospital, Shandong, 277100, China.

Biochemical and Biophysical Research Communications
|October 1, 2021
PubMed
Abstract

Insights

Long non-coding RNA ASMTL-AS1 promotes osteosarcoma progression by sponging miR-342-3p, leading to increased ADAM9. Silencing ASMTL-AS1 inhibits tumor growth and enhances apoptosis in osteosarcoma.

Area of Science:

  • Molecular Oncology
  • Cancer Biology
  • Genetics

Background:

  • The expression and function of long non-coding RNA ASMTL antisense RNA 1 (ASMTL-AS1) in osteosarcoma (OS) remain largely uncharacterized.
  • Osteosarcoma is a primary bone malignancy with significant unmet clinical needs.

Purpose of the Study:

  • To investigate the expression pattern of ASMTL-AS1 in osteosarcoma.
  • To elucidate the role of ASMTL-AS1 in regulating the malignant behaviors of osteosarcoma cells.
  • To identify the underlying molecular mechanism by which ASMTL-AS1 exerts its effects in osteosarcoma.

Main Methods:

  • ASMTL-AS1 expression levels were quantified in osteosarcoma tissues and cell lines using TCGA database and a local cohort.
  • Loss-of-function experiments (ASMTL-AS1 ablation) were performed to assess its impact on osteosarcoma cell proliferation, migration, invasion, and apoptosis in vitro.
  • In vivo tumor growth was evaluated after ASMTL-AS1 silencing.
  • Mechanistic studies involved bioinformatics analysis, luciferase reporter assays, RNA immunoprecipitation, and rescue experiments to explore the interaction between ASMTL-AS1, microRNA-342-3p (miR-342-3p), and ADAM metallopeptidase domain 9 (ADAM9).

Main Results:

  • ASMTL-AS1 expression was significantly upregulated in osteosarcoma tissues and cell lines.
  • Silencing ASMTL-AS1 suppressed osteosarcoma cell proliferation, migration, and invasion, while promoting apoptosis in vitro.
  • ASMTL-AS1 knockdown inhibited tumor growth in vivo.
  • Mechanistically, ASMTL-AS1 functions as a competing endogenous RNA (ceRNA) for miR-342-3p, thereby increasing the expression of its target gene, ADAM9. Inhibition of miR-342-3p or upregulation of ADAM9 could reverse the anti-tumor effects of ASMTL-AS1 silencing.

Conclusions:

  • ASMTL-AS1 plays a crucial role in promoting osteosarcoma progression.
  • The oncogenic function of ASMTL-AS1 is mediated through the ASMTL-AS1/miR-342-3p/ADAM9 axis.
  • Targeting the ASMTL-AS1/miR-342-3p/ADAM9 pathway may represent a potential therapeutic strategy for osteosarcoma.
Keywords:
Long non-coding RNAOS therapySMTL antisense RNA 1Therapeutic target

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