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PI3K/AKT/mTORC1-signaling pathway plays a role in induction of autophagy by type I interferons

Wednesday, November 06, 2013 — Poster Session I

4:00 p.m. – 6:00 p.m.

FAES Academic Center (Upper-Level Terrace)




  • H. Schmeisser
  • S.B. Fey
  • J. Horowitz
  • E.R. Fischer
  • C.A. Balinsky
  • K. Miyake
  • J. Bekisz
  • A.L. Snow
  • K.C. Zoon


Autophagy is a stress-induced cellular recycling mechanism that occurs at a basal level in all eukaryotic cells. Type I interferons are cytokines that have the ability to induce antiviral, antiproliferative and immunomodulatory activities in cells. Recently, we found that treatment with IFN-alpha2c and IFN-beta induces autophagy in Daudi B cells, starting at 24 h as indicated by an increase of autophagy markers LC3-II, Atg5-Atg12 complexes, and a decrease of p62. Higher levels of LC3-II were also detected 48 h post IFN-alpha2c treatment in HeLa S3, MDA-MB-231, T98G and A549 cell lines. The increase in expression of autophagy markers correlated with inhibition of mTORC1 activity in Daudi cells. Treatment of Daudi and T98G cells with IFN-alpha2c in combination with either rapamycin (mTORC1 inhibitor) or LY294002 (PI3K inhibitor) increased the level of LC3-II, indicating that PI3K/AKT/mTORC1 signaling pathway may affect IFN-induced autophagy in Daudi and T98G cells. The role of mTOR and factors upstream of mTOR in Type I IFN-induced autophagy was confirmed by siRNA knockdown experiments. The presence of autophagosomes was shown using transmission electron microscopy. In conclusion, our findings demonstrate a novel function of Type I IFN as inducer of autophagy in a variety of cancer cell lines.

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