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LncRNA GMDS-AS1 inhibits lung adenocarcinoma development by regulating miR-96-5p/CYLD signaling

Ming Zhao1, Xiao-Feng Xin1, Jian-Ya Zhang1

  • 1Department of Respiratory Medicine, Jinling Hospital, Second Military Medical University, Nanjing, China.

Cancer Medicine
|December 21, 2019
PubMed

Insights

Long noncoding RNA GMDS-AS1 acts as a tumor suppressor in lung adenocarcinoma (LUAD) by regulating the miR-96-5p/CYLD axis. Upregulating GMDS-AS1 inhibits LUAD cell proliferation and promotes apoptosis, offering a new therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Lung cancer, particularly lung adenocarcinoma (LUAD), remains a significant global health threat.
  • Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in tumorigenesis, but their specific mechanisms in LUAD require further elucidation.
  • Identifying novel molecular targets is crucial for developing effective LUAD therapies.

Purpose of the Study:

  • To investigate the role of lncRNA GMDS-AS1 in the development of lung adenocarcinoma.
  • To elucidate the molecular mechanism underlying GMDS-AS1's function in LUAD, focusing on its interaction with microRNAs and downstream targets.
  • To explore the potential of the GMDS-AS1/miR-96-5p/CYLD axis as a therapeutic strategy for LUAD.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to assess GMDS-AS1 expression in LUAD tissues and cells.
  • In vitro (cell culture) and in vivo (animal models) experiments to evaluate the effects of GMDS-AS1 upregulation on LUAD cell proliferation and apoptosis.
  • Bioinformatic analysis and luciferase reporter assays to confirm the interaction between GMDS-AS1, miR-96-5p, and CYLD.
  • Western blotting and immunohistochemistry to detect protein expression levels.

Main Results:

  • GMDS-AS1 expression was significantly downregulated in LUAD tissues and cells compared to normal controls.
  • Overexpression of GMDS-AS1 suppressed LUAD cell proliferation and induced apoptosis both in vitro and in vivo.
  • GMDS-AS1 was identified as a target of miR-96-5p, and it functions as a competing endogenous RNA (ceRNA) to upregulate CYLD expression by sponging miR-96-5p.
  • The GMDS-AS1/miR-96-5p/CYLD regulatory network was confirmed to play a critical role in LUAD cell proliferation and apoptosis.

Conclusions:

  • GMDS-AS1 functions as a tumor suppressor in LUAD.
  • The ceRNA network involving GMDS-AS1, miR-96-5p, and CYLD is a key regulator of LUAD progression.
  • Targeting the GMDS-AS1/miR-96-5p/CYLD axis offers a promising new avenue for LUAD targeted therapy.
Keywords:
CYLDlncRNA GMDS-AS1lung adenocarcinomamiR-96-5p

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