Investigation of Autophagic STING Regulation in Cisplatin Response in Lung Cancer Cell Lines
Project no. 23219 · Status: Kapanmış · 2021
Summary
<p>Lung cancer ranks second among cancer-related deaths. Non-Small Cell Lung Cancer (NSCLC); It constitutes ≌83% of the cases and is treated by surgical resection and chemo-radiotherapy according to the stage. Cisplatin, a platinum-based drug, is firstline chemotherapeutic used in the treatment of NSCLC. It has been observed that the cGAS-STING signalling pathway, which is responsible for the innate immune response, is activated in patients treated with cisplatin. The cGAS-STING pathway works as an important regulator of inflammation in conditions such as infection, cellular stress and tissue damage. At the same time, the cGAS-STING pathway has been shown to be important for the control of malignant transformation and tumour</p><p>progression. Recent studies indicate that there is an interaction between the STING protein and autophagy. It is known that autophagy increases during the development of cisplatin resistance in NSCLC. However, it is unclear how the STING-autophagy interaction occurs in the formation of the chemotherapy response. In our study; it was aimed to investigate the relationship between STING and autophagy in the cisplatin response of NSCLC cell lines with (Calu1) and without (H2030) STING expression. Experiments conducted in this direction have revealed the connection of autophagy</p><p>with STING expression and its effect on the formation of cisplatin response in NSCLC cell lines. We show that the mechanism of STING-mediated autophagy and the immunogenic effects of the cGAS-STING pathway may have the potential to shed light on new ways of treatment.</p>