SIRT7 deficiency promoted cuproptosis-mediated mitochondrial dysfunction and inhibited malignant development of cervical cancer
To investigate the impact of SIRT7 on the development of cervical cancer and its relationship with cuproptosis in cervical cancer. HeLa and SiHa cells were transfected with lentiviruses for SIRT7 overexpression and knockdown. The effects of SIRT7 on cervical cancer cell proliferation, apoptosis, invasion, and migration were analyzed using CCK8, plate cloning, flow cytometry, Transwell assays, and scratch assays. To verify the relationship between SIRT7 and cuproptosis, we utilized cuproptosis inhibitors and activators. Immunofluorescence, transmission electron microscope, flow cytometry, ELISA, and Western blot were used to analyze copper ion content, mitochondrial ultrastructure, cellular reactive oxygen species, mitochondrial membrane potential, pyruvate levels, cell viability and the cuproptosis-related proteins. SIRT7 enhanced the proliferation, migration, and invasion of HeLa and SiHa cells, inhibited apoptosis, and promoted cervical cancer growth. Knocking down SIRT7 caused cuproptosis of HeLa and SiHa cells, characterized by increased Cu SIRT7 was recognized as an oncogene in cervical cancer, which boosted cervical cancer cell proliferation and invasion, lowered intracellular copper levels, and prevented cuproptosis. SIRT7 downregulation triggered cuproptosis, inhibiting tumor cell growth.