Abstract 4709: Loss of GPSM2 promotes the metastasis of non-small cell lung cancer by inducing the expression of Snail

Background/Aims: Non-small cell lung cancer (NSCLC) is the leading global cause of cancer-related death. Due to the lack of reliable diagnostic or prognostic biomarkers, the prognosis of NSCLC remains poor. Consequently, there is an urgent need to explore the mechanisms underlying this condition in order to identify effective biomarkers. G protein signaling modulator 2 (GPSM2) is widely recognized as a determinant of mitotic spindle orientation. However, its role in cancer, especially NSCLC, remains uncertain. Methods: Tissue microarray (TMA) were used to compare differences in GPSM2 expression, and its relationship with clinical characteristics and prognosis. Wound healing assay, transwell assay and lung metastatic mice model were used to explore the biological function of GPSM2 on NSCLC cells in vitro and in vivo. Western blot and immunohistochemistry were conducted to investigate the potential pathways of GPSM2. Results: In this study, we found that GPSM2 was downregulated in NSCLC tissues and was correlated with a poor prognosis,and the expression status of GPSM2 was a favorable independent prognostic factor(HR = 0.222; 95% CI = 0.052 - 0.959; P = 0.044). Furthermore, the knockdown of GPSM2 promoted NSCLC cell metastasis in vitro and in vivo and accelerated the process of epithelial-to-mesenchymal transition (EMT). Mechanistically, we demonstrated that silencing GPSM2 induced cell metastasis and EMT via the ERK/GSK-3β/Snail pathway. Conclusion: These results confirm that GPSM2 plays an important role in NSCLC. Moreover, GPSM2, as an independent prognostic factor, may be a potential prognostic biomarker and drug target for NSCLC. Citation Format: Bofang Liu, Mingming Deng, Jingdong Zhang, Feifei Li, Weidong Han, Hongming Pan. Loss of GPSM2 promotes the metastasis of non-small cell lung cancer by inducing the expression of Snail [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 4709.