Based on in vivo and in vitro experiments validation: lncRNA MIR210HG inhibits esophageal squamous cell carcinoma and correlates with autophagy and apoptosis

Abstract

Background: Esophageal squamous cell carcinoma (ESCC) is a prevalent cancer that affects many people. The high death rate is still caused by ineffective early diagnostic and treatment methods. While the long non-coding RNA MIR210HG has been associated with several malignancies, its role in ESCC remains unclear. This study aims to explore the function of lncRNA MIR210HG in the pathogenesis of ESCC. Methods: We performed a pan-cancer analysis of lncRNA MIR210HG expression across various malignancies using the TCGA database, and we looked into the relationship between MIR210HG and the predictive survival of patients with ESCC. Moreover, we investigated MIR210HG's biological role using GO, KEGG, and GSEA enrichment analysis. In relation to MIR210HG, we also examined immune cell infiltration, immune checkpoint expression levels, tumor microenvironment (TME) features, and therapy sensitivity. To get more insight into the connection between lncRNA MIR210HG and ESCC, we assessed related gene and protein expression using Western blotting and RT-qPCR. To evaluate the proliferation, invasion, migration, apoptosis, and autophagy of ESCC cells, various techniques were employed, including EdU proliferation tests, wound healing assays, cell colony formation, transwell assays, flow cytometry, and an established xenograft mouse model. Results: lncRNA MIR210HG was found to be underexpressed in ESCC, and patients with higher expression levels of lncRNA MIR210HG exhibited increased survival rates. Overexpression of the lncRNA MIR210HG inhibited the proliferation, invasion, and migration of ESCC cells both in vitro and in vivo. Moreover, lncRNA MIR210HG was positively correlated with the P53 signaling pathway and influenced apoptosis and autophagy. Conclusion: In summary, lncRNA MIR210HG is a key gene affecting prognosis and immunity in ESCC and may influence apoptosis and autophagy through the P53 signaling pathway, offering new insights for the treatment of ESCC.