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Milk makes lysosomes lethal.

Shefali Krishna1, Michael Overholtzer1

  • 1Cell Biology Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA and at Louis V. Gerstner Jr. Graduate School of Biomedical Sciences, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.

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This summary is machine-generated.

Signal transducer and activator of transcription 3 (Stat3) triggers cell death during mammary gland involution. Stat3 causes milk fat globule phagocytosis, destabilizing lysosomes and releasing proteases.

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Area of Science:

  • Cell biology
  • Molecular biology
  • Physiology

Background:

  • Signal transducer and activator of transcription 3 (Stat3) is a key transcription factor involved in various cellular processes.
  • Stat3 has been implicated in regulating cell death and lysosome function during mammary gland involution.

Purpose of the Study:

  • To elucidate the precise mechanism by which Stat3 induces lysosome membrane permeabilization during post-lactation mammary gland involution.
  • To investigate the role of milk fat globule phagocytosis in Stat3-mediated cell death.

Main Methods:

  • In vivo studies of mammary gland involution.
  • Analysis of Stat3 signaling pathways.
  • Lysosome membrane permeabilization assays.
  • Investigation of phagocytosis of milk fat globules.

Main Results:

  • Stat3 activation directly leads to the phagocytosis of milk fat globules within mammary epithelial cells.
  • Phagocytosis of milk fat globules destabilizes the lysosome membrane.
  • Destabilized lysosomes release cathepsin proteases, initiating cell death pathways.

Conclusions:

  • Stat3-induced milk fat globule phagocytosis is a novel mechanism driving lysosome membrane permeabilization.
  • This process contributes significantly to cell death during mammary gland involution.
  • Targeting Stat3 or milk fat globule phagocytosis may offer therapeutic strategies for controlling cell death in relevant physiological contexts.