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DHRS2 mediates cell growth inhibition induced by Trichothecin in nasopharyngeal carcinoma

Xiangjian Luo1,2,3,4, Namei Li5,6,7, Xu Zhao5,6,7

  • 1Key Laboratory of Carcinogenesis and Invasion, Chinese Ministry of Education, Department of Radiology, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, People's Republic of China. luocsu@hotmail.com.

Journal of Experimental & Clinical Cancer Research : CR
|July 12, 2019
PubMed
Abstract

Insights

Activating Dehydrogenase/reductase member 2 (DHRS2) can inhibit nasopharyngeal carcinoma (NPC) cell growth by altering lipid metabolism. The compound trichothecin (TCN) shows potential therapeutic benefits against NPC by upregulating DHRS2.

Area of Science:

  • Oncology
  • Metabolomics
  • Molecular Biology

Background:

  • Cancer is characterized by uncontrolled cell growth and proliferation, often involving altered cellular metabolism.
  • Dehydrogenase/reductase member 2 (DHRS2), part of the short-chain alcohol dehydrogenase/reductase (SDR) superfamily, influences intermediary metabolism and lipid signaling.
  • DHRS2 expression is associated with inhibited cell proliferation, migration, and quiescence in various cancers.

Purpose of the Study:

  • To investigate the role of DHRS2 in nasopharyngeal carcinoma (NPC) cell proliferation and lipid metabolism.
  • To identify metabolic changes associated with DHRS2 overexpression in NPC.
  • To evaluate the anti-tumor effects of trichothecin (TCN) on NPC by examining its impact on DHRS2 expression.

Main Methods:

  • Cell proliferation was assessed using MTS, 5-ethynyl-2'-deoxyuridine (EdU), and colony formation assays.
  • Lipid metabolite profiling was performed using gas chromatography-mass spectrometry (GC/MS).
  • RNA sequencing and differential gene expression analysis were employed to study TCN's mechanism of action.

Main Results:

  • DHRS2 overexpression was found to alter lipid metabolite profiles, leading to cell cycle arrest and growth inhibition in NPC cells.
  • Trichothecin (TCN) demonstrated in vitro and in vivo efficacy in inhibiting NPC growth.
  • TCN exerts its anti-tumor effects by upregulating DHRS2 expression in NPC.

Conclusions:

  • Reprogramming lipid homeostasis through DHRS2 activation presents a potential therapeutic strategy for NPC.
  • TCN shows promise as a therapeutic agent for NPC by targeting DHRS2.
  • TCN can serve as a valuable tool for further elucidating the biological functions of DHRS2.
Keywords:
Cell cycleDHRS2Lipid metabolismNasopharyngeal carcinomaTrichothecin

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