ArticleCurrent medicinal chemistry2026
Reduced Expression of LINC01515 Suppresses Proliferation and Invasion of Lung Adenocarcinoma Cells via Modulation of the miR-33a-5p/HMGA2 Signaling Axis.
Article in Current medicinal chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
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4 authors.
Funding
Abstract
objectiveThis study examined the regulatory mechanisms and functional significance of LINC01515 in lung adenocarcinoma (LUAD) cells.
methodsAssociations between LINC01515 levels and patient survival were analyzed using TCGA data, and qRT-PCR was employed to assess LINC01515 transcript levels in both LUAD tissues (n = 15) and cell lines. Following LINC01515 silencing, changes in migration, proliferation, cellular viability, and invasion were evaluated using colony formation, CCK-8, and Transwell assays. Bioinformatics predictions of relationships among LINC01515, miR-33a-5p, and HMGA2 were confirmed using dual-luciferase reporter assays. Functional cellular experiments further verified that LINC01515 modulates both growth and motility via the miR-33a-5p/HMGA2 regulatory axis, and mouse xenograft models were employed to determine the effects of LINC01515 depletion on tumor development.
resultsCompared with matched normal controls, LINC01515 levels were markedly higher in LUAD tissues (p<0.01). Moreover, both cellular and animal functional tests revealed that LINC01515 silencing significantly decreased cell motility, colony-forming capacity, proliferation, and invasive potential. Further mechanistic investigations showed that LINC01515 acts as a competing endogenous RNA by sequestering miR-33a-5p, thereby alleviating the suppression of HMGA2 expression. Moreover, rescue assays confirmed that the regulatory interplay among LINC01515, miR-33a-5p, and HMGA2 is a key determinant of LUAD cell proliferation and motility. DISCUSSION: These data identify LINC01515 as an oncogenic driver of LUAD via a cytoplasmic ceRNA mechanism that derepresses HMGA2 through miR-33a-5p. Clinically, measuring LINC01515 may aid risk stratification and prognosis, and therapeutically, targeting LINC01515 or restoring the miR-33a-5p/HMGA2 balance represents a tractable axis to curb LUAD growth and dissemination, extending the lncRNA-based framework for precision oncology.
conclusionLINC01515 is predominantly distributed in the cytoplasm of LUAD cells and promotes oncogenic behavior through modulation of the miR-33a-5p/HMGA2 axis, suggesting the potential of LINC01515 as a biomarker and target in LUAD management.
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