ArticleJournal of thoracic disease2022
LINC00152 knockdown suppresses tumorigenesis in non-small cell lung cancer via sponging miR-16-5p.
Article in Journal of thoracic disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Investigation of the possible effects of LncRNA CYTOR on the molecular mechanisms of metastasis and Hippo signaling pathways in Triple-negative and Cisplatin-resistant breast cancer cell lines.Medical oncology (Northwood, London, England) · 2025Article
- LINC01980 promotes the malignant progression of lung squamous carcinoma by targeting miR-204-3p.Hereditas · 2025Article
- Quantitative determination of intracellular miRNA content using dual gold and iron nanoreporters and single particle ICP-ToF-MS.Mikrochimica acta · 2025Article
- circ_SPEF2 Regulates the Balance of Treg Cells by Regulating miR-16-5p/BACH2 in Lymphoma and Participates in the Immune Response.Tissue engineering and regenerative medicine · 2023Article
- Various LncRNA Mechanisms in Gene Regulation Involving miRNAs or RNA-Binding Proteins in Non-Small-Cell Lung Cancer: Main Signaling Pathways and Networks.International journal of molecular sciences · 2023Review
- CYTOR Promotes Proliferation of Lung Cancer Cell by Targeting miR-103a-3p to Upregulate HMGB1.Molecular biotechnology · 2023Article
- Transcriptomics data mining to uncover signature genes in head and neck squamous cell carcinoma: a bioinformatics analysis and RNA-sequencing based validation.American journal of cancer research · 2023Article
- Screening of four signature genes for clinical testing through bioinformatics and in vitro methods in head and neck squamous cell carcinoma.American journal of cancer research · 2023Article
- Long non-coding RNA LINC00152 in cancer: Roles, mechanisms, and chemotherapy and radiotherapy resistance.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Non-small cell lung cancer (NSCLC) is one of the most aggressive types of cancer worldwide. It has been reported that long non-coding RNAs (lncRNAs) are involved in the pathogenesis of NSCLC. In addition, LINC00152 is known to be upregulated in NSCLC. However, the mechanism underlying the effect of LINC00152 on NSCLC tumorigenesis remains to be elucidated. Methods: In the present study, cell viability, apoptosis and invasion were investigated by CCK-8, flow cytometry and Transwell assays, respectively. Reverse transcription‑quantitative polymerase chain reaction and Western blotting were performed to determine the mRNA and protein expression levels. In addition, the association between LINC00152, microRNA (miR)-16-5p and BCL2-like 2 (BCL2L2) was evaluated using a dual-luciferase assay. Results: The results demonstrated that LINC00152-knockdown significantly attenuated the viability of NSCLC cells via promoting cell apoptosis. In addition, the migration and invasion ability of NSCLC cells was also decreased following transfection of cells with LINC00152 siRNA. Furthermore, miR-16-5p inhibitor or BCLCL2-overexpression reversed LINC00152 siRNA-induced NSCLC cell growth inhibition. Conclusions: The findings of the present study demonstrated that LINC00152-silencing suppressed NSCLC tumorigenesis via regulating the miR-16-5p/BCL2L2 axis. Therefore, linc00152 has the potential as a molecular marker and may be a potential target for the treatment of non-small cell lung cancer.
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