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TIPRL potentiates survival of lung cancer by inducing autophagy through the eIF2α-ATF4 pathway

Su-Jin Jeon1,2, Jun-Ho Ahn1,3, Debasish Halder1

  • 1Genome Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, Yuseong-gu, Daejeon, Republic of Korea.

Cell Death & Disease
|December 22, 2019
PubMed

Insights

The TOR signaling pathway regulator-like (TIPRL) protein enhances autophagy in non-small cell lung cancer (NSCLC), promoting cancer cell survival. Inhibiting TIPRL may offer a new therapeutic strategy for lung cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cellular Biology

Background:

  • Autophagy is crucial for cancer cell survival by clearing damaged components.
  • Identifying novel regulators of autophagy is key for developing new anticancer therapies.

Purpose of the Study:

  • To investigate the role of the TOR signaling pathway regulator-like (TIPRL) protein in non-small cell lung cancer (NSCLC) autophagy.
  • To explore TIPRL as a potential drug target for lung cancer treatment.

Main Methods:

  • Examined the association between TIPRL and autophagy in NSCLC.
  • Investigated TIPRL's interaction with eukaryotic initiation factor 2α (eIF2α) and its effect on the eIF2α-ATF4 pathway.
  • Assessed the impact of TIPRL depletion on apoptosis and autophagic clearance in NSCLC cells and xenografts.

Main Results:

  • TIPRL upregulation in NSCLC potentiates autophagy, aiding cancer cell survival by clearing stress.
  • TIPRL interacts with eIF2α, leading to its phosphorylation and activation of the eIF2α-ATF4 pathway, inducing autophagy.
  • TIPRL depletion increases apoptosis and reduces autophagic clearance, an effect enhanced by 2-deoxy-D-glucose treatment in xenografts.

Conclusions:

  • TIPRL acts as a regulator of autophagy in NSCLC.
  • TIPRL is a promising drug target for developing novel lung cancer therapies.

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