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Loss of RND3/RHOE controls entosis through LAMP1 expression in hepatocellular carcinoma

Sara Basbous1, Lydia Dif1, Camille Dantzer1

  • 1University of Bordeaux, INSERM, BRIC, U1312, Bordeaux, France.

Cell Death & Disease
|January 13, 2024
PubMed

Insights

Loss of Rnd3 protein induces cell-in-cell entosis in liver cancer, a process linked to tumor metastasis. This finding reveals entosis as a potential therapeutic target for hepatocellular carcinoma.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Biology

Background:

  • Entosis, a cellular process forming cell-in-cell structures, is prevalent in various cancers.
  • The specific role and regulation of entosis in hepatocellular carcinoma (HCC) remain incompletely understood.

Purpose of the Study:

  • To investigate the role of Rnd3 (RhoE) in entosis within hepatocellular carcinoma.
  • To elucidate the molecular mechanisms and stages of Rnd3-induced entosis.
  • To explore the correlation between entosis and tumor progression in HCC.

Main Methods:

  • Induction of entosis via Rnd3 silencing in HCC cell models.
  • Characterization of entosis stages and molecular regulators.
  • Proteomic profiling of entotic cells.
  • Analysis of patient samples for correlation between entosis and metastatic potential.

Main Results:

  • Loss of Rnd3 efficiently induces entosis in HCC.
  • Entosis induced by Rnd3 silencing depends on the RhoA/ROCK pathway but not E-cadherin.
  • LAMP1 is upregulated in Rnd3-silenced cells and plays a role in entosis.
  • A positive correlation exists between entotic cell presence and tumor metastatic potential in HCC patients.

Conclusions:

  • Rnd3 loss is a key driver of entosis in hepatocellular carcinoma.
  • Entosis, regulated by RhoA/ROCK and involving LAMP1, contributes to liver tumor progression.
  • Entosis represents a novel therapeutic target for HCC treatment and diagnosis.

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