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Updated: Aug 8, 2025

Author Spotlight: Regulation and Dysregulation of ER-Mitochondria Contacts — Implications for Neurodegenerative Disease Pathogenesis
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Key genes expressed in mitochondria‑endoplasmic reticulum contact sites in cancer (Review)

Sophia Themistocleous1, Panayiota Christodoulou1, Theodora-Christina Kyriakou1

  • 1School of Medicine, European University Cyprus, 2404 Nicosia, Cyprus.

Oncology Reports
|March 3, 2023
PubMed

Insights

Mitochondrial proteins at contact sites regulate cell fate by controlling calcium. Disruptions in these proteins and calcium flux impact cell death and cancer, offering therapeutic targets.

Area of Science:

  • Cellular Biology
  • Mitochondrial Function
  • Calcium Signaling

Background:

  • Mitochondrial activity and mitochondrial-endoplasmic reticulum contact sites (MERCSs) are crucial for cell fate, influencing ATP production, metabolism, and calcium (Ca2+) homeostasis.
  • Disruptions in MERCSs or mitochondrial physiology, particularly Ca2+ flux, are linked to altered autophagy and apoptosis.
  • MERCS proteins play a key role in regulating these cellular processes.

Approach:

  • This review synthesizes findings from numerous studies on MERCS proteins.
  • It examines how these proteins modulate Ca2+ across membranes, affecting anti- and pro-apoptotic properties.
  • The review explores the role of mitochondrial proteins in cancer development and cell death.

Key Points:

  • MERCS proteins regulate cell fate through calcium signaling.
  • Alterations in MERCS protein function and Ca2+ flux are implicated in apoptosis and autophagy.
  • Mitochondrial proteins are identified as critical factors in cancer development and cell survival/death.

Conclusions:

  • MERCS proteins are key regulators of cell death and survival via calcium modulation.
  • Dysfunctional MERCS proteins and calcium signaling contribute to cancer.
  • Targeting mitochondrial proteins at MERCSs presents a potential therapeutic strategy for cancer.
Keywords:
Ca2+ singlingMERCSMERCS genescancer

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