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Down-regulation of MIAT suppresses osteosarcoma progression by acting as a ceRNA for miR-141-3p to regulate

Q Ji1, J Zhu, C-L Fang

  • 1Department of Orthopaedics, Huishan District People's Hospital, Wuxi, Jiangsu, China. huangjie0451@tom.com.

European Review for Medical and Pharmacological Sciences
|March 21, 2020
PubMed
Abstract

Insights

Long non-coding RNA MIAT promotes osteosarcoma progression by regulating SIX1 via miR-141-3p and the PI3K/AKT pathway. MIAT inhibition offers a potential therapeutic strategy for osteosarcoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Osteosarcoma (OS) is a common bone cancer.
  • Long non-coding RNA myocardial infarction associated transcript (MIAT) is implicated in various cancers.
  • The precise role of MIAT in OS progression is not fully understood.

Purpose of the Study:

  • To elucidate the mechanism of MIAT in osteosarcoma (OS) progression.
  • To investigate the relationship between MIAT, miR-141-3p, and SIX1 in OS.
  • To explore the potential of targeting MIAT for OS treatment.

Main Methods:

  • Quantitative real-time PCR and Western blot to assess MIAT and SIX1 expression.
  • Cellular assays (MTT, flow cytometry, trans-well) to evaluate OS cell behavior.
  • Bioinformatics, luciferase reporter assays, and Western blot to analyze molecular interactions and pathway activation (PI3K/AKT).

Main Results:

  • MIAT and SIX1 were upregulated in OS tissues and cells.
  • MIAT or SIX1 knockdown inhibited OS cell viability, migration, and invasion while promoting apoptosis.
  • MIAT promoted SIX1 expression by sponging miR-141-3p, thereby activating the PI3K/AKT pathway.

Conclusions:

  • MIAT knockdown suppresses OS progression by inhibiting the PI3K/AKT pathway via the miR-141-3p/SIX1 axis.
  • MIAT acts as a oncogenic factor in osteosarcoma.
  • Targeting MIAT presents a potential therapeutic avenue for osteosarcoma treatment.

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