LINC01352 Inhibits Lung Adenocarcinoma Progression by Modulating the miR‐425‐5p/SRSF11 Pathway

Abstract

Lung adenocarcinoma (LUAD), as the most common subtype of non‐samll cell lung cancer, is highly malignant and associated with a poor overall prognosis for patients, making it imperative to further investigate its molecular mechanisms of pathogenesis. This study aims to clarify the role of LINC01352 in the malignant progression of lung adenocarcinoma (LUAD). LINC01352 expression in LUAD versus normal tissue was analyzed using StarBase and GEPIA databases. RT‐qPCR was employed to explore the levels of LINC01352, miR‐425‐5p, and SRSF11 in102 clinically collected LUAD tissue samples. Cell proliferation was assessed using the CCK‐8 assay, while cell migration and invasion capabilities were examined via Transwell experiments. DLR and RIP experiments were performed to validate the target relationships between LINC01352 and miR‐425‐5p, as well as SRSF11 and miR‐425‐5p. The level of LINC01352 decreased in LUAD, and enhancing LINC01352 inhibited the malignant phenotype of LUAD cells. LINC01352 binds to miR‐425‐5p. Increasing miR‐425‐5p expression offset the inhibitory impacts of LINC01352 overexpression on the malignant behavior of LUAD cells. Furthermore, SRSF11 is a target of miR‐425‐5p, and its expression in LUAD tissues showed a significant inverse relationship with miR‐425‐5p. LINC01352 exerts tumor‐suppressive function in LUAD through the miR‐425‐5p/SRSF11 axis, thereby inhibiting malignant progression of LUAD. This study indicates that targeting the LINC01352/miR‐425‐5p/SRSF11 pathway may represent a promising therapeutic strategy for LUAD.