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Published on: July 21, 2018
LINC00365 inhibited lung adenocarcinoma progression and glycolysis via sponging miR-429/KCTD12 axis
Cheng-Wei Zhang1, Bin Zhou1, Yan-Chao Liu1
1Department of Thoracic Surgery, Capital Medical University Electric Power Teaching Hospital, Beijing, China.
Abstract:
This study researched the function of long non-coding RNA LINC00365 in lung adenocarcinoma (LAD) progression. LINC00365, miR-429, and KCTD12 expression in the LAD clinical tissues and cells were detcetd by qRT-PCR and Western blot. LINC00365, miR-429, and KCTD12 effects on H1975 cells malignant phenotype were detected by cell counting kit-8 assay, clone formation experiment, Transwell experiment, and glycolysis. Dual luciferase reporter gene assay and RNA pull-down assay were implemented. LINC00365 effect on H1975 cells in vivo growth was detected. LINC00365 was low expressed in the LAD patients and cells, associating with poor outcome. LINC00365 up-regulation attenuated H1975 cells proliferation, migration, invasion, glycolysis and in vivo growth. LINC00365 inhibited KCTD12 expression by sponging miR-429. miR-429 up-regulation and KCTD12 down-regulation partial reversed LINC00365 inhibition on H1975 cells malignant phenotype. Thus, LINC00365 inhibited LAD progression and glycolysis via targeting miR-429/KCTD12 axis. LINC00365 might be a potential candidate for LAD target treatment clinically.
Insights
Long non-coding RNA LINC00365 is downregulated in lung adenocarcinoma (LAD), inhibiting cancer progression and glycolysis. LINC00365 targets the miR-429/KCTD12 axis, offering potential for LAD treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Lung adenocarcinoma (LAD) is a major cause of cancer mortality.
- The role of long non-coding RNAs (lncRNAs) in LAD pathogenesis is increasingly recognized.
- Identifying novel therapeutic targets for LAD is crucial.
Purpose of the Study:
- To investigate the function of LINC00365 in lung adenocarcinoma progression.
- To elucidate the molecular mechanism underlying LINC00365's role in LAD.
- To assess LINC00365 as a potential therapeutic target for LAD.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) and Western blot to assess gene and protein expression.
- Cell proliferation, migration, invasion, and glycolysis assays to evaluate cellular phenotype.
- Dual luciferase reporter gene and RNA pull-down assays to confirm molecular interactions.
- In vivo studies to assess the effect of LINC00365 on tumor growth.
Main Results:
- LINC00365 expression was significantly downregulated in LAD tissues and cells, correlating with poor prognosis.
- Upregulation of LINC00365 suppressed LAD cell proliferation, migration, invasion, glycolysis, and in vivo tumor growth.
- LINC00365 acted as a molecular sponge for miR-429, inhibiting KCTD12 expression.
- Overexpression of miR-429 or knockdown of KCTD12 partially reversed the inhibitory effects of LINC00365.
Conclusions:
- LINC00365 inhibits LAD progression and glycolysis by targeting the miR-429/KCTD12 axis.
- LINC00365 demonstrates potential as a novel therapeutic target for lung adenocarcinoma.
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