C11orf53 Promotes the Progression of Small Cell Lung Cancer by Regulating Glucose Metabolism

Small cell lung cancer (SCLC), the most malignant subtype of lung cancer, is a major cause of death among lung cancer patients. Drug resistance, high recurrence, and limitations of surgery are all obstacles to SCLC treatment. Consequently, clarifying the underlying mechanism of SCLC progression and identifying potential targets for therapeutic intervention are of paramount significance for improving the clinical outcomes of SCLC patients. C11orf53 has been demonstrated to play a crucial role in the NCI-H526 cell activity. However, few studies have focused on how C11orf53 affects the activity of NCI-H526 cells and the corresponding regulatory pathways. Herein, our study shows that C11orf53 affects the viability and proliferation of SCLC NCI-H526 cells by influencing the glycolytic pathway. We established the C11orf53 overexpression and knockdown systems in the NCI-H526 cell line with C11orf53-specific small-interfering RNA and lentivirus to assess the effects of C11orf53 on the activity and proliferation of NCI-H526 cells. Furthermore, the NCI-H526 cells with C11orf53 knockdown and overexpression were utilized to elucidate the molecular mechanism of C11orf53. Our study shows that C11orf53 knockdown significantly reduced the viability and proliferation of NCI-H526 cells. Additionally, adenosine triphosphate levels, glucose consumption, lactate secretion, and the expression of key enzymes involved in the glycolytic pathway were markedly decreased in NCI-H526 cells. These findings confirmed that the effect of C11orf53 on the activity and proliferation of NCI-H526 cells is mediated by its role in regulating cellular glycolysis.