This study examines the role of VASN in rectal cancer, finding that its high expression is associated with pulmonary metastasis and chemotherapy resistance. By establishing stable overexpression and knockdown cell lines of VASN, the authors further validated VASN's role in promoting cancer cell migration, invasion, and proliferation. Both in vitro and in vivo results show that VASN overexpression significantly enhances cancer cell invasion and reduces sensitivity to chemotherapeutic agents. The experimental methods include transfection of the VASN gene using lentiviral vectors, establishment of stable cell lines through G418 resistance selection, and verification of VASN overexpression via Western blot and qPCR.

The LBX1 gene, located near single nucleotide polymorphisms highly associated with adolescent idiopathic scoliosis susceptibility, is considered one of the strongest candidate genes for the disease mechanism. The study found that LBX1 deletion not only causes spinal deformities but also affects lean body mass, suggesting LBX1's potential role in energy metabolism. This study aimed to test this hypothesis by analyzing the phenotype of LBX1-deficient skeletal muscle in mice, focusing on energy metabolism. Results showed that LBX1-deficient mice exhibited greater resistance to high-fat diet-induced obesity, despite similar food intake to control mice. Mutant mice also demonstrated better glucose tolerance, higher maximal aerobic capacity, and increased core temperature. Furthermore, LBX1 overexpression reduced glucose uptake in cultured cells. Together, the data indicate that LBX1 acts as a negative regulator of energy metabolism, with its deletion increasing systemic energy expenditure, leading to lean body mass. The study also suggests a potential association between LBX1 dysfunction and lean body mass in adolescent idiopathic scoliosis patients.

This study investigates the role and pathogenesis of serine- and arginine-rich splicing factor 10 (SRSF10) in colorectal cancer (CRC). Bioinformatics analysis predicted SRSF10 gene expression in CRC patients, and functional experiments involving SRSF10 knockdown and overexpression were conducted using CCK8, Transwell, scratch assays, and flow cytometry. SRSF10 knockdown inhibited CRC cell proliferation and migration, promoted apoptosis, and altered DNA replication, while SRSF10 overexpression enhanced proliferation and migration and caused cell cycle changes. Notably, high SRSF10 expression reduced glucose uptake in cultured cells, further indicating its role as a negative regulator of energy metabolism. The study also revealed changes in the RFC5 gene in CRC cells after SRSF10 knockdown, with SRSF10 increasing the exon 2-AS1(S) transcript variant of RFC5, promoting abnormal splicing of exon 2 and advancing CRC progression. These findings suggest that SRSF10 may serve as an important target for CRC clinical diagnosis and treatment.