PLCG2 promotes cell survival and mitophagy of small cell lung cancer via regulating VCP

Small cell lung cancer (SCLC) is a highly aggressive form of lung cancer that is characterized by rapid growth. PLCG2 is an enzyme that plays a crucial role in intracellular signal transduction pathways. This study aims to discover the role of PLCG2 in SCLC and the underlying mechanism. Relative expression of PLCG2 was detected by reverse transcription-quantitative PCR and Western blot. Cell viability, proliferation, and apoptosis were assessed by cell counting kit-8, colony formation, and flow cytometry assays. Mitophagy-related protein levels were analyzed by Western blot. RNA immunoprecipitation and dual-luciferase reporter assays were used to analyze the interaction between PLCG2 and VCP . A xenograft mouse model was established to analyze the role of PLCG2 in vivo . Results showed that PLCG2 was upregulated in SCLC tissues and cells, with high diagnostic potential. Besides, PLCG2 deficiency inhibited cell survival and mitophagy and promoted apoptosis in SCLC cells. In addition, PLCG2 interacted with VCP , and VCP overexpression reversed the inhibitory effects of PLCG2 silencing. In vivo , PLCG2 silencing suppressed SCLC tumor growth. In conclusion, PLCG2 is a promising biomarker for SCLC diagnosis and might be a potential therapeutic target, with its interaction with VCP playing a role in SCLC cell survival and mitophagy.