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The Recombinant Fragment of Human κ-Casein Induces Cell Death by Targeting the Proteins of Mitochondrial Import in Breast Cancer Cells. | LitMetric

AI Article Synopsis

  • Breast cancer remains a prevalent cancer among women, and effective therapies are crucial for treatment.
  • The study investigates how RL2, a recombinant fragment of human κ-Casein, causes cell death in breast cancer cells, focusing on its impact on mitochondrial function and ATP levels.
  • Key findings reveal that RL2 interacts with the mitochondrial import protein TOM70, leading to reduced ATP production and cell death, suggesting that this interaction could be a potential target for new breast cancer therapies.

Article Abstract

Breast cancer is still one of the most common cancers for women. Specified therapeutics are indispensable for optimal treatment. In previous studies, it has been shown that RL2, the recombinant fragment of human κ-Casein, induces cell death in breast cancer cells. However, the molecular mechanisms of RL2-induced cell death remain largely unknown. In this study, mechanisms of RL2-induced cell death in breast cancer cells were systematically investigated. In particular, we demonstrate that RL2 induces loss of mitochondrial membrane potential and cellular ATP loss followed by cell death in breast cancer cells. The mass spectrometry-based screen for RL2 interaction partners identified mitochondrial import protein TOM70 as a target of RL2, which was subsequently validated. Further to this, we show that RL2 is targeted to mitochondria after internalization into the cells, where it can also be found in the dimeric form. The importance of TOM70 and RL2 interaction in RL2-induced reduction in ATP levels was validated by siRNA-induced downregulation of TOM70, resulting in the partial rescue of ATP production. Taken together, this study demonstrates that RL2-TOM70 interaction plays a key role in RL2-mediated cell death and targeting this pathway may provide new therapeutic options for treating breast cancer.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7352597PMC
http://dx.doi.org/10.3390/cancers12061427DOI Listing

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