CD8+ T Cells in Association with SCD1 Regulate Cervical Cancer and Tumour Microenvironment Correlation Research

Objective To explore new strategies for treating cervical cancer and tumour microenvironment correlation. Methods Clinical significance and prognostic impact of SCD (Stearoyl-CoA Desaturase ) in cervical cancer through bioinformatics analysis of the GTEx project and the TCGA database. Immunohistochemical analysis of SCD1 expression in clinical cervical cancer tissues and normal cervical tissues. CCK-8 assay, cell cycle, transwell assay, western blotting, transmission electron microscopy, reactive oxygen species (ROS) detection, lipid peroxidation detection, and ferroptosis analysis were performed to reveal the role and underlying mechanisms in cervical cancer cell line (HeLa & CaSki). Results SCD1 is highly expressed in clinical cervical cancer tissues, especially in advanced cancer. Knockdown SCD1 inhibits proliferation and migration in cervical cancer cells. Knockdown SCD1 induces ferroptosis in cervical cancer cells by upregulating ROS, Fe2+, lipid peroxidation, ferroptosis indicator (Acyl-CoA synthetase long chain family member 4, ACSL4) and downregulating of ferroptosis indicator (Glutathione Peroxidase 4, GPX4), mitochondrial membrane potential (MMP). Transmission electron microscopy revealed morphological changes in mitochondria after knockdowning SCD1. 72 cervical cancer cases (63 stage I-II and 9 stage III-IV) were retrospectively analysed and confirmed statistical significant difference in expression of SCD1 in early and advanced cervical cancer. CD8+ T cell expression was significantly reduced in cancer tissues with high SCD1 expression. There was significant heterogeneity in CD8+ T cell expression in peripheral blood and cancer tissues. Conclusion This study suggested that knockdown SCD1 acts as a novel ferroptosis-inducing agent in cervical cancer cells, and the relationship between SCD1 and CD8⁺ T cells is inversal.