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Updated: Dec 1, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
LINC00518 Interference Inhibits Non-Small Cell Lung Cancer by Upregulating miR216b-5p Expression
Yuanyuan Ren1,2, Huadong Zhu3, Song Han4
1Department of Oncology, People's Hospital of Taizhou, Taizhou, Jiangsu Province 225300, China.
Introduction:
Non-small cell lung cancer (NSCLC) accounts for the majority of lung cancer cases, and effective treatment for this disease is still lacking. This study aimed to explore the potential role of LINC00518 and miR216b-5p on cell proliferation and tumor growth in NSCLC.
Methods:
The expression of LINC00518, miR216b-5p, MMP7, and MMP9 in NSCLC cell lines was determined by RT-qPCR analysis, which was also used to confirm the transfection effects. After transfection, proliferation, clone-formation ability, migration, and invasion of NSCLC cells were detected by CCK8, clone-formation, wound-healing, and transwell assays, respectively. Western blot analysis was used to detect the expression of MMP7, MMP9, Ki67, and PCNA. A xenograft model was constructed by subcutaneous injection of transfected NSCLC cells into nude mice.
Results:
The results indicated that LINC00518 expression was increased and miR216b-5p expression decreased in NSCLC cell lines, and A549 cells were chosen for the next experiments. LINC00518 interference inhibited proliferation, invasion, and migration of A549 cells, together with the progression of NSCLC in vivo. In addition, LINC00518 directly targeted miR216b-5p. Downregulation of miR216b-5p weakened the inhibitory effect of LINC00518 interference on proliferation, invasion, and migration of A549 cells, as well as progression of NSCLC in vivo.
Discussion:
In conclusion, LINC00518 interference inhibits NSCLC, which is partially reversed by downregulation of miR216b-5p expression.
Insights
Interfering with LINC00518 inhibits non-small cell lung cancer (NSCLC) progression by affecting cell proliferation and metastasis. This effect is partly reversed by reducing miR216b-5p levels.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Non-small cell lung cancer (NSCLC) remains a significant health challenge with limited effective treatments.
- Understanding the molecular mechanisms driving NSCLC progression is crucial for developing novel therapeutic strategies.
Purpose of the Study:
- To investigate the functional roles of LINC00518 and miR216b-5p in NSCLC.
- To elucidate the regulatory relationship between LINC00518 and miR216b-5p in NSCLC cells.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) to assess gene expression.
- Cellular assays including CCK8, clone formation, wound healing, and Transwell assays to evaluate proliferation, migration, and invasion.
- Western blot analysis for protein expression.
- In vivo xenograft models in nude mice.
Main Results:
- LINC00518 was upregulated, while miR216b-5p was downregulated in NSCLC cell lines.
- LINC00518 interference suppressed NSCLC cell proliferation, migration, invasion, and tumor growth in vivo.
- LINC00518 directly targets miR216b-5p.
- Downregulation of miR216b-5p partially reversed the inhibitory effects of LINC00518 interference.
Conclusions:
- LINC00518 interference demonstrates therapeutic potential for NSCLC.
- The LINC00518/miR216b-5p axis plays a critical role in NSCLC progression.
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