NNT-AS1 modulates prostate cancer cell proliferation, apoptosis and migration through miR-496/DDIT4 axis

Changlei Yao1, Xianghua Cheng1, Xiuquan Guo1

  • 1Department of Urinary Surgery, People's Hospital of Rizhao, No.126, Tai an Street, Dong Gang District, Rizhao, 276826 Shandong China.

Cancer Cell International
|September 28, 2020
PubMed
Abstract

Insights

Long non-coding RNA NNT-AS1 promotes prostate cancer (PCa) progression by upregulating DDIT4 expression via sponging miR-496. This finding offers a potential therapeutic target for PCa treatment.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) are increasingly recognized as key regulators in prostate cancer (PCa) development.
  • The specific role of lncRNA nicotinamide nucleotide transhydrogenase antisense RNA 1 (NNT-AS1) in PCa remains largely unexplored.

Purpose of the Study:

  • To investigate the functional involvement of NNT-AS1 in the progression of prostate cancer.
  • To elucidate the molecular mechanism underlying NNT-AS1's action in PCa cells.

Main Methods:

  • Quantitative reverse transcription PCR (RT-qPCR) was used to measure RNA expression levels.
  • In vitro functional assays evaluated PCa cell viability, proliferation, apoptosis, and migration.
  • RNA pull-down and luciferase reporter assays were employed to determine molecular interactions.

Main Results:

  • NNT-AS1 expression was significantly upregulated in PCa cells.
  • Depletion of NNT-AS1 inhibited PCa cell viability, proliferation, and migration, while inducing apoptosis.
  • NNT-AS1 was found to sequester miR-496, leading to increased expression of DNA damage inducible transcript 4 (DDIT4).
  • Rescue experiments confirmed that DDIT4 overexpression or miR-496 inhibition reversed the effects of NNT-AS1 depletion.

Conclusions:

  • NNT-AS1 promotes malignant phenotypes in PCa cells.
  • This promotion occurs via the NNT-AS1/miR-496/DDIT4 axis.
  • NNT-AS1 represents a potential therapeutic target for prostate cancer.

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