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CD95 and CD95L promote and protect cancer stem cells

Author

Listed:
  • Paolo Ceppi

    (Feinberg School of Medicine, Northwestern University)

  • Abbas Hadji

    (Feinberg School of Medicine, Northwestern University)

  • Frederick J. Kohlhapp

    (Feinberg School of Medicine, Northwestern University)

  • Abhinandan Pattanayak

    (Feinberg School of Medicine, Northwestern University)

  • Annika Hau

    (Feinberg School of Medicine, Northwestern University)

  • Xia Liu

    (School of Medicine, Case Western Reserve University)

  • Huiping Liu

    (School of Medicine, Case Western Reserve University)

  • Andrea E. Murmann

    (Feinberg School of Medicine, Northwestern University)

  • Marcus E. Peter

    (Feinberg School of Medicine, Northwestern University)

Abstract

CD95 (APO-1/Fas) is a death receptor used by immune cells to kill cancer cells through induction of apoptosis. However, the elimination of CD95 or its ligand, CD95L, from cancer cells results in death induced by CD95R/L elimination (DICE), a type of cell death that resembles a necrotic form of mitotic catastrophe suggesting that CD95 protects cancer cells from cell death. We now report that stimulation of CD95 on cancer cells or reducing miR-200c levels increases the number of cancer stem cells (CSCs), which are more sensitive to induction of DICE than non-CSC, while becoming less sensitive to CD95-mediated apoptosis. In contrast, induction of DICE or overexpression of miR-200c reduces the number of CSCs. We demonstrate that CSCs and non-CSCs have differential sensitivities to CD95-mediated apoptosis and DICE, and that killing of cancer cells can be maximized by concomitant induction of both cell death mechanisms.

Suggested Citation

  • Paolo Ceppi & Abbas Hadji & Frederick J. Kohlhapp & Abhinandan Pattanayak & Annika Hau & Xia Liu & Huiping Liu & Andrea E. Murmann & Marcus E. Peter, 2014. "CD95 and CD95L promote and protect cancer stem cells," Nature Communications, Nature, vol. 5(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6238
    DOI: 10.1038/ncomms6238
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