LINC00313 functions as an oncogenic propellant and immunosuppressive marker in lung adenocarcinoma.

Abstract

Background: Despite advances in treatments, the prognosis for lung adenocarcinoma (LUAD) remains poor, underscoring the urgent need to identify novel therapeutic strategies. This study was conducted to investigate the potential role of LINC00313 as a biomarker and therapeutic target for LUAD.

Methods: Databases GEPIA2 and GEO were used to analyze LINC00313 expression and prognosis. Analyses of pathways associated with LINC00313, and its relationships with immune infiltration, checkpoint therapy response and drug response were conducted using different bioinformatics tools. siRNA transfection, qRT-PCR, transwell and colony formation assays were performed on LUAD cells (A549).

Results: LINC00313 is significantly upregulated in LUAD, and its expression is associated with high-grade cancer, poor prognosis and metastasis. In vitro studies showed that silencing LINC00313 reduced LUAD cell migration, invasion, and colony formation. Bioinformatics analyses indicated that LINC00313 expression was negatively associated with immune cell infiltration and the efficacy of immune checkpoint inhibitor therapy. Sensitivity analysis of chemotherapeutic drugs found that high expression of LINC00313 attenuated the effect of chemotherapeutic drugs like cisplatin, dabrafenib and lapatinib on LUAD.

Conclusions: In conclusion, LINC00313 holds potential as a valuable biomarker and therapeutic target for the treatment of LUAD. However, further research is warranted to fully elucidate its clinical applications.