The mechanism of LSM2 in the progression of live hepatocellular carcinoma was analyzed based on bioinformatics

Abstract Comprehensive analysis the expression and probable function of LSM2 in Live hepatocellular carcinoma (LIHC), and validation via in vitro experiments. Integrated use of database resources like TIMER2.0, GEPIA, LinkedOmics to examine the differential expression, survival prognosis, clinical pathological features, and functional enrichment of LSM2 in LIHC. The expression level of LSM2 in LIHC tissues and adjacent tissues was proven via immunohistochemical staining. Employing shRNA interference techniques to reduce the expression level of LSM2 in LIHC. The biological function of LSM2 in LIHC was detected by cell proliferation, cell cloning, cell scratch, cell migration, and invasion experiments in vitro. TIMER2.0 and GEPIA indicated that LSM2 was highly expressed in various cancers and was strongly associated with survival rates in patients with LIHC, cholangiocarcinoma, breast cancer, and renal clear cell carcinoma. LSM2 was highly expressed in LIHC, which was closely associated to the clinicopathological characteristics of patients, and the overall survival rate and disease-free survival rate of patients with high expression of LSM2 were lower than those with low expression of LSM2. Functional enrichment results revealed that LSM2 was involved to ribosome formation, DNA replication, cell cycle, metabolic processes, JAK-STAT signaling pathways, and FoxO signaling pathways. Compared with the paracancerous tissues, the expression of LSM2 in LIHC tissues was higher. Knockdown of LSM2 inhibited the proliferation, migration, and invasion of LIHC cells in in vitro experiments. LSM2 was highly expressed in LIHC and was related to a poor prognosis. Knockdown of LSM2 could inhibit the proliferation, migration, and invasion of LIHC cells.