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Upregulation of long non-coding RNA NNT-AS1 promotes osteosarcoma progression by inhibiting the tumor suppressive

Changhui Li1, Shouyun Zhang1, Tongguo Qiu2

  • 1a Department of Orthopedics , People's Hospital of Rizhao , Shandong , China.

Cancer Biology & Therapy
|November 30, 2018
PubMed
Abstract

Insights

Nicotinamide nucleotide transhydrogenase antisense RNA 1 (NNT-AS1) promotes osteosarcoma (OS) by downregulating miR-320a, leading to increased expression of key proteins like beta-catenin and RUNX2. This study reveals NNT-AS1 as a potential therapeutic target for OS treatment.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Osteosarcoma (OS) is a primary bone malignancy with a complex molecular landscape.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development and progression.
  • Understanding the specific functions of lncRNAs like NNT-AS1 in OS is crucial for identifying novel therapeutic targets.

Purpose of the Study:

  • To elucidate the role and underlying mechanism of NNT-AS1 in osteosarcoma.
  • To investigate the interaction between NNT-AS1 and microRNA-320a (miR-320a) in OS cells.
  • To assess the impact of NNT-AS1 on OS cell proliferation, migration, invasion, and tumor formation.

Main Methods:

  • Bioinformatic analysis to predict miR-320a as a target of NNT-AS1.
  • In vitro studies involving NNT-AS1 overexpression and knockdown in OS cell lines to assess cellular functions.
  • RT-qPCR and western blotting to evaluate the expression of NNT-AS1, miR-320a, and related proteins (beta-catenin, RUNX2, IGF-1R, c-Myc, Cyclin D1, MMP13).
  • In vivo xenograft models to evaluate tumor formation and molecular changes.
  • Transfection with miR-320a mimics and inhibitors to confirm the regulatory pathway.

Main Results:

  • NNT-AS1 overexpression enhanced OS cell proliferation, survival, and migration in vitro and tumor formation in vivo.
  • NNT-AS1 knockdown exhibited opposite effects.
  • NNT-AS1 expression positively correlated with beta-catenin, RUNX2, IGF-1R, c-Myc, Cyclin D1, MMP13, and Akt phosphorylation, and inversely correlated with miR-320a.
  • miR-320a mimic transfection inhibited NNT-AS1-induced promoting effects, while miR-320a inhibitor partially rescued the effects of NNT-AS1 knockdown.

Conclusions:

  • NNT-AS1 acts as a cancer-promoting lncRNA in osteosarcoma.
  • NNT-AS1 exerts its oncogenic function by downregulating miR-320a.
  • This downregulation leads to increased protein levels of beta-catenin, RUNX2, and IGF-1R, and activation of the Akt pathway, promoting osteosarcoma progression.
Keywords:
NNT-AS1long noncoding RNAmiR-320aosteosarcoma

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