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Long non-coding RNAs MACC1-AS1 and FOXD2-AS1 mediate NSD2-induced cisplatin resistance in esophageal squamous cell

Wenhua Xue1,2, Zhibo Shen1,3,4, Lifeng Li3,4

  • 1Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Molecular Therapy. Nucleic Acids
|February 8, 2021
PubMed

Insights

Nuclear receptor-binding SET domain protein 2 (NSD2) promotes cisplatin resistance in esophageal squamous cell carcinoma (ESCC) by upregulating MACC1-AS1. Targeting NSD2 and MACC1-AS1 may improve chemotherapy efficacy in ESCC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Nuclear receptor-binding SET domain (NSD) proteins are histone lysine methyltransferases implicated in cancer progression.
  • The specific role of NSD proteins in esophageal squamous cell carcinoma (ESCC) and their impact on chemotherapy resistance are not well understood.

Purpose of the Study:

  • To investigate the role of NSD proteins, particularly NSD2, in cisplatin resistance in ESCC.
  • To elucidate the molecular mechanisms underlying NSD2-mediated cisplatin resistance, focusing on its interaction with long non-coding RNAs.

Main Methods:

  • Comparative analysis of NSD protein expression in cisplatin-resistant and parental ESCC cell lines.
  • Functional studies involving ectopic expression and knockdown of NSD2 and MACC1-AS1 in ESCC cells.
  • Assessment of cisplatin sensitivity, apoptosis, proliferation, and colony formation.
  • In vivo studies using EC109 xenograft tumor models.
  • Correlation analysis of NSD2 and MACC1-AS1 expression with clinical data from ESCC patients.

Main Results:

  • NSD2 was significantly upregulated in cisplatin-resistant ESCC cells.
  • Overexpression of NSD2 conferred cisplatin resistance and enhanced cell survival, while NSD2 knockdown sensitized cells to cisplatin.
  • NSD2 promoted cisplatin resistance by upregulating the long non-coding RNA MACC1-AS1.
  • MACC1-AS1 overexpression also promoted ESCC proliferation and cisplatin resistance.
  • Clinically, MACC1-AS1 was upregulated in ESCC tissues and correlated with reduced patient survival, with a positive correlation to NSD2 expression.

Conclusions:

  • NSD2 plays a critical role in mediating cisplatin resistance in ESCC, partly through the induction of MACC1-AS1.
  • The NSD2-MACC1-AS1 axis represents a potential therapeutic target for overcoming cisplatin resistance in esophageal squamous cell carcinoma.
  • Targeting this pathway could enhance the effectiveness of cisplatin-based chemotherapy in ESCC patients.
Keywords:
MACC1-AS1NSD2apoptosiscisplatin resistanceesophageal cancer

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