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

IF 3.6 3区医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Biochemical and Molecular Toxicology Pub Date : 2026-10-15 DOI:10.1002/jbt.71109

Xiaoxiao Ma, Ling Liu, Fang Fang

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引用次数: 0

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.

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LINC01352通过调节miR-425-5p/SRSF11通路抑制肺腺癌进展

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来源期刊

Journal of Biochemical and Molecular Toxicology 生物-毒理学

CiteScore

5.80

自引率

2.80%

发文量

277

审稿时长

6-12 weeks

期刊介绍： The Journal of Biochemical and Molecular Toxicology is an international journal that contains original research papers, rapid communications, mini-reviews, and book reviews, all focusing on the molecular mechanisms of action and detoxication of exogenous and endogenous chemicals and toxic agents. The scope includes effects on the organism at all stages of development, on organ systems, tissues, and cells as well as on enzymes, receptors, hormones, and genes. The biochemical and molecular aspects of uptake, transport, storage, excretion, lactivation and detoxication of drugs, agricultural, industrial and environmental chemicals, natural products and food additives are all subjects suitable for publication. Of particular interest are aspects of molecular biology related to biochemical toxicology. These include studies of the expression of genes related to detoxication and activation enzymes, toxicants with modes of action involving effects on nucleic acids, gene expression and protein synthesis, and the toxicity of products derived from biotechnology.