PLCE1 is a poor prognostic marker and may promote immune escape from osteosarcoma by the CD70-CD27 signaling pathway.

Phospholipase C epsilon 1 (PLCE1) is involved in the pathogenesis of many cancers. However, the biological role of PLCE1 in osteosarcoma (OS) is still poorly understood. The prognostic survival analysis was performed on the PLCE1gene in the TARGET data set and the differential expression of PLCE1 in OS tissue and normal bone tissue on the tissue chip was detected by immunohistochemistry. Spearman's rank correlation coefficient analysis was implemented to explore the relationship between PLCE1 and immune genes. Finally, PLCE1 was silenced to explore its biological function in OS cells. The results of tissue chip immunohistochemistry showed that PLCE1 expression in OS tissue was higher than in normal bone tissue. The survival curve of PLCE1 and its corresponding receiver operating characteristic curve (ROC) showed that PLCE1 had a significant effect on the survival status of patients with OS and that the prognosis of patients with high PLCE1 expression was relatively poor. Spearman's rank correlation coefficient analysis and qRT-PCR assays found that PLCE1 may promote immune escape from OS via CD70-CD27 signaling pathway. Silencing of PLCE1 causes the following biological behaviors of OS cells: it promotes apoptosis, inhibits proliferation of OS cells, and inhibits the ability of cell migration and invasion. PLCE1 is a poor prognostic marker and a potential key factor affecting the immune status of the OS tumor microenvironment.

The biological function and clinical significance of STIL in osteosarcoma.

BACKGROUND: SCL/TAL1 interrupting locus (STIL) is associated with the progression of several tumors; however, the biological role of STIL in osteosarcoma remains poorly understood. METHODS: In this study, the clinical significance of STIL in osteosarcoma was analyzed by gene chip data recorded in public databases. STIL expression was silenced in osteosarcoma cell lines to observe the effects on proliferation, apoptosis, invasion, and migration. Differentially expressed genes (DEGs) in the osteosarcoma chip were analyzed using The Limma package, and STIL co-expressed genes were obtained via the Pearson correlation coefficient. The potential molecular mechanism of STIL in osteosarcoma was further explored by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. RESULTS: Osteosarcoma was associated with higher STIL expression compared to the control samples, and the standardized mean difference (SMD) was 1.52. STIL also had a good ability to distinguish osteosarcoma from non-osteosarcoma samples [area under the curve (AUC) = 0.96]. After silencing STIL, osteosarcoma cell proliferation decreased, apoptosis increased, and the migratory and invasion ability decreased. A total of 294 STIL differentially co-expressed genes were screened, and a bioinformatics analysis found that differentially co-expressed genes were primarily enriched in the cell signaling pathways. The protein-protein interaction (PPI) network indicated that the hub differentially co-expressed genes of STIL were CDK1, CCNB2, CDC20, CCNA2, BUB1, and AURKB. CONCLUSIONS: STIL is associated with osteosarcoma proliferation and invasion, and may be promote the progression of osteosarcoma by regulating the expression of CDK1, CCNB2, CDC20, CCNA2, BUB1 and AURKB.

Knockdown of RPL34 suppresses osteosarcoma cell proliferation likely through EIF3/FAU signaling pathway.

BACKGROUND: This study aims to explore the effect of knockdown of the ribosomal protein L34 (RPL34) on osteosarcoma cell proliferation through EIF3/FAU. METHODS: The mRNA expression levels of RPL34, EIF3A, EIF3F, EIF3G, UBA52, UBC, and FAU were quantified using quantitative real-time PCR (qRT-PCR) in two human cell lines: the hFOB1.19 osteoblast cell line and the Saos-2 osteosarcoma cell line. The qRT-PCR analysis was performed to confirm the shRNA-mediated depletion of RPL34, and a western blot analysis was done to confirm the knockdown of protein levels. qRT-PCR was also used to examine the effects of RPL34 knockdown on the above genes. RESULTS: The mRNA expression levels of RPL34, EIF3A, EIF3G, UBA52, UBC, and FAU were increased in the Saos-2 cells relative to the hFOB1.19 osteoblast cells. EIF3F expression was decreased in Saos-2 cells relative to hFOB1.19 cells. Knockdown of RPL34 mRNA significantly suppressed EIF3A and EIF3F expression and significantly up-regulated FAU expression in the Saos-2 cell line, but there were no remarkable differences in the relative expression in the EIF3G, UBA52, and UBC genes. CONCLUSIONS: Knockdown of RPL34 suppresses osteosarcoma cells proliferation probably through EIF3A, EIF3F, and FAU.