Related Experiment Video

Updated: May 31, 2026

Revealing the Ferroptotic Phenotype of Medulloblastoma
04:01

Revealing the Ferroptotic Phenotype of Medulloblastoma

Published on: March 15, 2024

USP52-RAB11FIP5 axis suppresses ferroptosis by repressing transferrin receptor recycling in head and neck squamous

Anjiang Sun1, Xin Xia1, Xiuxian Niu2

  • 1State Key Laboratory of Cellular Stress Biology, Cancer Research Center, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen 361102, China; School of Medicine, Xiamen University, Xiamen 361102, China.

Cell Reports
|May 28, 2026
PubMed

Insights

Researchers identified RAB11FIP5 as a key regulator of ferroptosis and cell proliferation in head and neck squamous cell carcinoma (HNSCC). This protein restricts iron uptake, impacting tumor growth and offering a potential therapeutic target for HNSCC.

Area of Science:

  • Oncology
  • Cell Death Mechanisms

Background:

  • Ferroptosis, an iron-dependent cell death, has tumor-suppressive roles but its regulation in head and neck squamous cell carcinoma (HNSCC) is unclear.
  • Understanding ferroptosis regulators is crucial for developing novel cancer therapies.

Purpose of the Study:

  • To identify key regulators of ferroptosis in HNSCC.
  • To elucidate the molecular mechanisms by which these regulators impact tumor growth and cell death.

Main Methods:

  • Investigated RAB11FIP5 function in HNSCC cell lines.
  • Utilized molecular biology techniques to study protein interactions and ubiquitination.
  • Performed in vitro proliferation assays and in vivo xenograft tumor models.

Main Results:

  • RAB11FIP5 was identified as a negative regulator of ferroptosis in HNSCC.
  • RAB11FIP5 restricts iron uptake by antagonizing transferrin receptor recycling.
  • USP52 stabilizes RAB11FIP5 by removing ubiquitin chains, impacting ferroptosis and cell proliferation.
  • RAB11FIP5 knockout suppressed tumor growth via ferroptosis-dependent and -independent pathways.

Conclusions:

  • RAB11FIP5 acts as a dual regulator of ferroptosis and cell proliferation in HNSCC.
  • Targeting RAB11FIP5 presents a promising therapeutic strategy for HNSCC treatment.
Keywords:
CP: cancerCP: cell biologyFerroptosisHNSCCRAB11ARAB11FIP5TFRCUSP52

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