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m6A-dependent regulation of DGUOK-AS1 by RBM15 and HNRNPH1 in lung adenocarcinoma

Menghao Yang1, Jiaen Wu1,2, Youjie Li1

  • 1Department of Biochemistry and Molecular Biology, Binzhou Medical University, Yantai, Shandong, China.

Iscience
|August 16, 2026
PubMed

Insights

This study reveals how deoxyguanosine kinase antisense RNA 1 (DGUOK-AS1) promotes lung adenocarcinoma (LUAD) progression. It highlights an m6A-dependent mechanism involving RBM15 and HNRNPH1 that stabilizes DGUOK-AS1, impacting LUAD cell growth and migration.

Area of Science:

  • Molecular Oncology
  • Non-coding RNA Biology
  • Cancer Genomics

Background:

  • Lung adenocarcinoma (LUAD) is a major cause of cancer mortality, necessitating deeper molecular insights.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development.
  • Understanding the regulatory networks in LUAD is crucial for developing targeted therapies.

Purpose of the Study:

  • To elucidate the regulatory mechanism of deoxyguanosine kinase antisense RNA 1 (DGUOK-AS1) in LUAD.
  • To investigate the role of DGUOK-AS1 in LUAD cell proliferation and migration.
  • To explore the molecular interactions and signaling pathways involving DGUOK-AS1.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to assess DGUOK-AS1 expression in LUAD cells and serum.
  • In vitro and in vivo functional assays to evaluate the impact of DGUOK-AS1 on LUAD progression.
  • RNA immunoprecipitation (RIP) and Western blot assays to investigate protein-RNA interactions and modifications (m6A).

Main Results:

  • DGUOK-AS1 expression was significantly upregulated in LUAD tissues and serum, correlating with LUAD.
  • DGUOK-AS1 overexpression promoted LUAD cell proliferation and migration in vitro and in vivo.
  • DGUOK-AS1 acts as a competing endogenous RNA for miR-2467-5p, modulating PRMT5 expression.
  • RNA-binding motif protein 15 (RBM15) enhances DGUOK-AS1 stability via m6A modification, facilitating heterogeneous nuclear ribonucleoprotein H1 (HNRNPH1) binding and degradation.
  • RBM15 knockdown suppressed LUAD malignancy via the miR-2467-5p/PRMT5 axis.

Conclusions:

  • DGUOK-AS1 plays a critical oncogenic role in LUAD progression.
  • An m6A-dependent mechanism involving RBM15 and HNRNPH1 regulates DGUOK-AS1 stability.
  • The DGUOK-AS1/miR-2467-5p/PRMT5 axis represents a potential therapeutic target for LUAD.
Keywords:
DGUOK-AS1HNRNPH1LUADPRMT5RBM15m6A

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