LINC00426, a novel m6A-regulated long non-coding RNA, induces EMT in cervical cancer by binding to ZEB1

Siyuan Shen1, Hua Jin2, Xing Zhang1

  • 1Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing, China.

Cellular Signalling
|July 1, 2023
PubMed
Abstract

Insights

LINC00426 promotes cervical cancer (CC) progression and drug resistance via m6A modification and the miR-200a-3p/ZEB1 axis. This lncRNA is a potential therapeutic target for CC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Cervical cancer (CC) remains a significant global health challenge.
  • Understanding the molecular mechanisms driving CC progression is crucial for developing effective therapies.

Purpose of the Study:

  • To elucidate the function and molecular mechanism of LINC00426 in CC.
  • To investigate LINC00426 as a potential therapeutic target for CC.

Main Methods:

  • Bioinformatics analysis of LINC00426 expression and patient prognosis.
  • In vitro cell function experiments to assess malignant phenotypes.
  • m6A modification analysis, luciferase reporter assays, and RIP assays to determine molecular interactions.
  • Cell viability assays to evaluate drug resistance.

Main Results:

  • LINC00426 is upregulated in CC, enhancing cell proliferation, migration, and invasion.
  • METTL3-mediated m6A modification promotes LINC00426 expression.
  • The LINC00426/miR-200a-3p/ZEB1 axis regulates epithelial-mesenchymal transition (EMT) in CC.
  • Overexpression of LINC00426 confers resistance to cisplatin and bleomycin, and sensitivity to imatinib.

Conclusions:

  • LINC00426 acts as an oncogenic long noncoding RNA (lncRNA) in CC, linked to m6A modification.
  • The LINC00426/miR-200a-3p/ZEB1 pathway is a key regulator of EMT in CC.
  • LINC00426 influences CC cell sensitivity to chemotherapy drugs, presenting a promising therapeutic target.

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