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Histones Methyltransferase NSD3 Inhibits Lung Adenocarcinoma Glycolysis Through Interacting with PPP1CB to Decrease

Yanling Zhou1,2, Xintong Peng3,4, Cheng Fang5

  • 1Department of Oncology, Institute of Medical Sciences, National Clinical Research Center for Geriatric Disorders, Institue of Medical Sciences, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|August 9, 2024
PubMed

Insights

Histone methyltransferase NSD3 suppresses lung adenocarcinoma growth and spread by inhibiting glycolysis. This study reveals NSD3

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Histone methyltransferase NSD3 (Nuclear Receptor SET Domain Containing 3) is frequently altered in cancers.
  • The role of NSD3 in cancer initiation and progression is not fully understood.

Purpose of the Study:

  • To investigate the function of NSD3 in lung adenocarcinoma.
  • To elucidate the mechanism by which NSD3 affects cancer progression.

Main Methods:

  • In vivo studies in lung adenocarcinoma models.
  • Analysis of NSD3 expression correlation with clinical features and survival.
  • Investigation of NSD3's effect on glycolysis, proliferation, migration, and invasion.
  • Protein-protein interaction studies involving NSD3, PPP1CB, and p-STAT3.
  • Assessment of environmental factors (CO2, pH) on protein phosphorylation.

Main Results:

  • Downregulated NSD3 levels correlate with poor prognosis in lung adenocarcinoma.
  • NSD3 inhibits tumor proliferation, migration, and invasion in vivo.
  • NSD3 suppresses glycolysis by reducing HK2 translation and glucose uptake.
  • NSD3 forms a complex with PPP1CB and p-STAT3 to dephosphorylate p-STAT3, inhibiting HK2 transcription.
  • PPP1CB phosphorylation is influenced by CO2 and pH levels.

Conclusions:

  • NSD3 plays a critical non-epigenetic role in suppressing lung adenocarcinoma.
  • NSD3 regulates STAT3-dependent glycolysis through the NSD3/PPP1CB/p-STAT3 pathway.
  • Targeting the NSD3/PPP1CB/p-STAT3 axis presents a potential therapeutic strategy for lung adenocarcinoma.
Keywords:
STAT3 signaling pathwayglycolysishistones methyltransferaselung adenocarcinoma

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