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Reduced mitochondrial Rab32 impairs mitochondria-endoplasmic reticulum contacts and inhibits apoptosis in

Xiacheng Sun1, Xiaoli Liu2, Qichao Huang2

  • 1National Demonstration Center for Experimental Basic Medical Science Education, Fourth Military Medical University, Xi'an, Shaanxi 710032, China; State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers and Department of Physiology and Pathophysiology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.

Pathology, Research and Practice
|May 12, 2026
PubMed

Insights

Mitochondria-endoplasmic reticulum contacts (MERCs) are crucial for liver cancer cells. Mitochondrial Rab32 maintains MERC integrity, impacting apoptosis and proliferation, suggesting MERC stabilization as a potential hepatocellular carcinoma (HCC) therapy.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Mitochondrial Biology

Background:

  • Mitochondria-endoplasmic reticulum contacts (MERCs) are vital for cellular calcium and apoptosis.
  • MERC dysfunction is linked to liver diseases, but its role in hepatocellular carcinoma (HCC) is unclear.

Purpose of the Study:

  • To investigate the role of mitochondrial Rab32 in maintaining MERC integrity in HCC cells.
  • To elucidate the mechanism by which Rab32 regulates MERCs and its impact on HCC progression.

Main Methods:

  • Investigated the localization and function of Rab32 in HCC cells.
  • Utilized protein kinase A (PKA) and PTPIP51 phosphorylation assays.
  • Assessed mitochondrial calcium (Ca²⁺) levels and reactive oxygen species (ROS) accumulation.
  • Employed a synthetic mitochondria-ER linker to restore MERC integrity.

Main Results:

  • Mitochondrial Rab32 is essential for maintaining MERC integrity in HCC.
  • Rab32 promotes PKA localization to mitochondria, facilitating PTPIP51 phosphorylation and MERC stability.
  • Rab32 deficiency disrupts MERCs, leading to decreased mitochondrial Ca²⁺ and increased ROS.
  • Restoring MERC integrity inhibited HCC cell proliferation and enhanced apoptosis.

Conclusions:

  • Mitochondrial Rab32 is a key regulator of MERC integrity and apoptosis in HCC.
  • Targeting Rab32 or stabilizing MERCs presents a potential therapeutic strategy for hepatocellular carcinoma (HCC).
Keywords:
ApoptosisHepatocellular carcinoma (HCC)Mitochondria–ER contactsRab32

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