Background

Lung adenocarcinoma (LUAD) remains one of the leading causes of cancer-related deaths worldwide, with limited therapeutic efficacy despite advances in treatment. Our study investigated the role of LINC00578 and its regulatory interaction with miR-153-5p in LUAD progression.

Methods

The expression levels of LINC00578 and miR-153-5p were assessed in LUAD tissues and adjacent normal tissues using quantitative real-time polymerase chain reaction. Associations between LINC00578 expression and clinicopathological features and patient prognosis were analyzed. Luciferase reporter assays, proliferation, migration, invasion, and apoptosis analyses, were conducted in LUAD cell lines (PC-9 and H1299) following modulation of LINC00578 and miR-153-5p expression.

Results

LINC00578 was significantly upregulated in LUAD tissues compared to adjacent normal tissues, whereas miR-153-5p was markedly downregulated. High LINC00578 expression was associated with lymph node metastasis, tumor-node-metastasis stage, and poor overall survival. Functional studies revealed that silencing LINC00578 inhibited LUAD cell proliferation, migration, and invasion while promoting apoptosis. Mechanistically, LINC00578 exerted its oncogenic effects by negatively regulating miR-153-5p expression. Inhibition of miR-153-5p reversed the tumor-suppressive effects induced by LINC00578 knockdown.

Conclusion

LINC00578 functions as an oncogenic long non-coding RNA in LUAD by promoting proliferation and metastasis through suppression of miR-153-5p. LINC00578 may serve as a novel prognostic biomarker for LUAD.

Search results

LINC00578 as a prognostic biomarker in lung adenocarcinoma via regulation of miR-153-5p