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Updated: Apr 29, 2026

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MARCH3 Inhibits Tumorigenesis and Enhances Paclitaxel Sensitivity in Nasopharyngeal Carcinoma by Ubiquitinating

Xinggu Luo1, Qingshan Jiang1, Zhifeng Liu1

  • 1Department of Otorhinolaryngology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.

Journal of Biochemical and Molecular Toxicology
|April 27, 2026
PubMed

Insights

Membrane-associated RING-CH-type finger 3 (MARCH3) inhibits nasopharyngeal carcinoma (NPC) progression by promoting the degradation of hexokinase 2 (HK2). Upregulating MARCH3 enhances sensitivity to paclitaxel (PTX) in NPC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Hexokinase 2 (HK2) is a key glycolytic enzyme implicated in human cancers, including nasopharyngeal carcinoma (NPC).
  • Understanding the regulatory mechanisms of HK2 is crucial for developing effective NPC therapies.

Purpose of the Study:

  • To investigate the role and underlying mechanism of HK2 in NPC progression.
  • To explore the relationship between HK2 and membrane-associated RING-CH-type finger 3 (MARCH3) in NPC.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR) and Western blot for HK2 and MARCH3 expression.
  • Cell proliferation, migration, invasion, and apoptosis assays (CCK-8, colony formation, wound healing, Transwell, flow cytometry).
  • Co-immunoprecipitation (Co-IP) and GST pull-down assays to validate protein interactions; in vivo studies for therapeutic efficacy.

Main Results:

  • HK2 expression was elevated, while MARCH3 expression was decreased in NPC tissues and cell lines.
  • HK2 knockdown suppressed NPC cell proliferation, migration, invasion, and glycolysis, while enhancing paclitaxel (PTX) sensitivity.
  • MARCH3 overexpression promoted HK2 ubiquitination and degradation, thereby reducing HK2 stability and inhibiting NPC progression.

Conclusions:

  • MARCH3 acts as a tumor suppressor in NPC by targeting HK2 for ubiquitination and degradation.
  • MARCH3 enhances NPC cell sensitivity to PTX, suggesting its potential as a therapeutic target for NPC treatment.
Keywords:
HK2MARCH3PTX sensitivitynasopharyngeal carcinomaproliferation

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