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Differential regulation of STING expression and cisplatin sensitivity by autophagy in non-small cell lung cancer

Sevim Aydemir1, Zafer Yildirim1, Busra Bara1

  • 1Faculty of Medicine, Department of Medical Biology, Ege University, Izmir, Türkiye.

Medical Oncology (Northwood, London, England)
|May 30, 2025
PubMed

Insights

The cGAS-STING pathway

Area of Science:

  • Cellular Biology
  • Immunology
  • Oncology

Background:

  • The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway is crucial for inflammatory responses and is activated by cisplatin.
  • Increased autophagy correlates with cisplatin resistance in non-small cell lung cancer (NSCLC), but the interplay between autophagy and STING in this context is unknown.

Purpose of the Study:

  • To investigate how modulating autophagy impacts STING expression and cisplatin sensitivity in NSCLC cells with varying basal STING levels.

Main Methods:

  • Autophagy was manipulated using chloroquine (inhibition) and serum starvation (induction) in Calu-1 and H2030 NSCLC cell lines.
  • STING expression, cGAS-STING pathway activation, interferon responses, and cisplatin sensitivity were assessed.

Main Results:

  • In Calu-1 cells (high basal STING), cisplatin increased STING, activated cGAS-STING, and induced interferon responses.
  • Autophagy inhibition enhanced cisplatin sensitivity by reducing STING and interferon activation.
  • Autophagy induction decreased cisplatin sensitivity, with serum starvation selectively increasing ISG15 expression.
  • H2030 cells (low basal STING) showed minimal responses to cisplatin or autophagy modulation.

Conclusions:

  • STING expression levels are critical determinants of autophagy-mediated responses to DNA-damaging chemotherapy in NSCLC.
  • Targeting the autophagy-STING axis may offer therapeutic strategies for NSCLC.
Keywords:
AutophagyChloroquineCisplatinNSCLCStarvationcGAS-STING

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