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Metastatic breast cancer cells are selectively dependent on the mitochondrial cristae-shaping protein OPA1

Antigoni Diokmetzidou1,2, Aurora Maracani1,2, Anna Pellattiero1,2

  • 1Department of Biology, University of Padova, Padova, Italy.

Cell Death & Disease
|July 21, 2025
PubMed

Insights

Optic Atrophy 1 (OPA1) is upregulated in metastatic breast cancer. Inhibiting OPA1 selectively targets these cancer cells, reducing their respiration, migration, and proliferation, offering a new therapeutic vulnerability.

Area of Science:

  • Mitochondrial biology
  • Cancer cell biology
  • Oncology

Background:

  • Optic Atrophy 1 (OPA1) is implicated in breast cancer chemoresistance.
  • The role of OPA1 in normal versus metastatic breast cancer cells is not fully understood.

Purpose of the Study:

  • To investigate the role of OPA1 in breast cancer progression and metastasis.
  • To determine if OPA1 inhibition selectively affects metastatic breast cancer cells.

Main Methods:

  • Utilized an isogenic model of normal, transformed, and metastatic breast cancer cells.
  • Assessed mitochondrial dynamics, respiration, proliferation, and migration.
  • Employed OPA1 inhibitors MYLS22 and Opitor-0.

Main Results:

  • OPA1 is upregulated in metastatic breast cancer cells, correlating with mitochondrial fragmentation and increased respiration.
  • OPA1 deletion selectively impaired metastatic cell respiration, proliferation, and migration.
  • OPA1 inhibition reduced migration and increased cell death in metastatic cells.

Conclusions:

  • OPA1 upregulation is a hallmark of metastatic breast cancer.
  • OPA1 represents a selective vulnerability in metastatic breast cancer cells.
  • Targeting OPA1 may offer a novel therapeutic strategy for metastatic breast cancer.

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