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LncRNA NEAT1 promotes dexamethasone resistance in multiple myeloma by targeting miR-193a/MCL1 pathway

Yilan Wu1, Han Wang2

  • 1School of Nursing, Fujian University of Traditional Chinese Medicine, Fujian 350122, People's Republic of China.

Journal of Biochemical and Molecular Toxicology
|December 6, 2017
PubMed

Insights

Dexamethasone resistance in multiple myeloma is a poor prognostic indicator. This study found that targeting NEAT1 can restore myeloma cell sensitivity to dexamethasone, offering a potential therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Dexamethasone (DEX) is a primary treatment for multiple myeloma (MM).
  • DEX resistance in MM correlates with poor patient outcomes.
  • Developing strategies to overcome DEX resistance is crucial for MM treatment.

Purpose of the Study:

  • To investigate the role of long non-coding RNA NEAT1 in DEX resistance in MM.
  • To elucidate the molecular mechanisms underlying DEX resistance involving NEAT1.

Main Methods:

  • Analysis of NEAT1 expression in DEX-resistant MM cell lines.
  • Investigating the relationship between NEAT1, miR-193a, and MCL1 expression.
  • Assessing the impact of NEAT1 knockdown and overexpression on DEX sensitivity.

Main Results:

  • NEAT1 was highly expressed in DEX-resistant MM cells and linked to poor prognosis.
  • Decreased miR-193a levels and increased MCL1 expression were observed during DEX resistance development.
  • NEAT1 knockdown enhanced DEX sensitivity in resistant cells, while overexpression induced resistance in sensitive cells.

Conclusions:

  • The NEAT1/miR-193a/MCL1 pathway is implicated in the development of DEX resistance in MM.
  • Targeting NEAT1 presents a potential strategy to improve DEX sensitivity in MM patients.
Keywords:
MCLdexamethasonelncRNA NEAT1miR-193amultiple myeloma

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