Related Experiment Video

Updated: Nov 6, 2025

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
08:55

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

11.0K

MLKL in cancer: more than a necroptosis regulator

Sofie Martens1,2, Jolien Bridelance1,2, Ria Roelandt1

  • 1Cell Death and Inflammation Lab, VIB Center for Inflammation Research, Ghent, Belgium.

Cell Death and Differentiation
|May 6, 2021
PubMed

Insights

Mixed lineage kinase domain-like protein (MLKL) executes necroptosis and has roles beyond cell death. This protein may influence cancer development and metastasis through both necroptosis-dependent and -independent functions.

Area of Science:

  • Cell Biology
  • Cancer Biology
  • Molecular Oncology

Background:

  • Mixed lineage kinase domain-like protein (MLKL) is the executioner of necroptosis, a regulated necrosis pathway.
  • Cancer cells can evade cell death, including necroptosis, and inflammation from necroptosis can promote tumor growth.
  • Emerging evidence highlights necroptosis-independent functions of MLKL in various cellular processes.

Purpose of the Study:

  • To review current knowledge and controversies surrounding MLKL in cancer.
  • To explore MLKL's structure, expression, mutations, and potential roles in cancer development and metastasis.
  • To discuss both necroptosis-dependent and -independent functions of MLKL in oncology.

Main Methods:

  • Literature review and analysis of existing research on MLKL.
  • Examination of MLKL expression patterns in relation to inflammation and tissue injury.
  • Discussion of reported MLKL mutations and their implications.

Main Results:

  • MLKL expression is upregulated by type I/II interferon, inflammation, and tissue injury.
  • MLKL exhibits diverse necroptosis-independent functions, including roles in receptor trafficking, autophagy, and immune regulation.
  • The precise role of MLKL in cancer, as a pro- or anti-cancer factor, remains under investigation.

Conclusions:

  • MLKL's multifaceted roles, encompassing both necroptosis execution and necroptosis-independent functions, suggest a complex involvement in cancer.
  • Understanding MLKL's regulation and functions is crucial for deciphering its impact on tumor progression and metastasis.
  • Further research is warranted to elucidate MLKL's precise contribution to cancer development and its potential as a therapeutic target.

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