ArticleOncoTargets and therapy2018
LINC00888 promoted tumorigenicity of melanoma via miR-126/CRK signaling axis.
Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- LINC00888 Promotes Gastric Cancer Growth and Metastasis by Sponging miR-145-5p to Regulate FZD7 Expression.Combinatorial chemistry & high throughput screening · 2026Article
- Novel Biological Strategies for Melanoma Therapy: A Focus on lncRNAs and Their Targeting.Cancers · 2025Review
- Pathogenic roles of long noncoding RNAs in melanoma: Implications in diagnosis and therapies.Genes & diseases · 2023Review
- STAT3-induced ZBED3-AS1 promotes the malignant phenotypes of melanoma cells by activating PI3K/AKT signaling pathway.RNA biology · 2021Article
- Epigenetic Silencing of MicroRNA-126 Promotes Cell Growth in Marek's Disease.Microorganisms · 2021Article
- Xmrks the Spot: Fish Models for Investigating Epidermal Growth Factor Receptor Signaling in Cancer Research.Cells · 2021Review
- LncRNA PAINT is associated with aggressive prostate cancer and dysregulation of cancer hallmark genes.International journal of cancer · 2021Article
- Elevated LINC01550 induces the apoptosis and cell cycle arrest of melanoma.Medical oncology (Northwood, London, England) · 2021Article
- Regulation of MethylaseDiabetes, metabolic syndrome and obesity : targets and therapy · 2021Review
- Cyclophilin A Inhibitor Debio-025 Targets Crk, Reduces Metastasis, and Induces Tumor Immunogenicity in Breast Cancer.Molecular cancer research : MCR · 2020Article
- Article
- Long Intergenic Noncoding RNA 00261 Acts as a Tumor Suppressor in Non-Small Cell Lung Cancer via Regulating miR-105/FHL1 Axis.Journal of Cancer · 2019Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesMelanoma is an aggressive skin cancer. Understanding the underlying mechanisms for melanomagenesis and identification of novel and effective melanoma treatment strategies are urgently necessary. The long-noncoding RNAs are considered as new essential players during cancer development, including the melanoma. MATERIALS AND
methodsIn this study, we first determined the expression of LINC00888 in tumor tissues and adjacent normal tissues from 28 patients with melanoma using quantitative polymerase chain reaction, and the correlation between the expression level of LINC00888 and the survival months was also examined. Next, we investigated the effect of LINC00888 on the proliferation, apoptosis, and invasion in the melanoma cells. Moreover, LINC00888-specific miRNA and target gene were further confirmed using the dual-luciferase reporter assay and Western blotting. Last, the tumorigenesis role of LINC00888 was also explored using tumor xenografts mouse model.
resultsElevated LINC00888 expression was found in melanoma specimens compared with adjacent normal tissues. The 4-year overall survival in melanoma patients with high expression of LINC00888 was substantially shorter than that in those with low expression of LINC00888. Knockdown of LINC00888 significantly inhibited the proliferation, apoptosis, epithelial-mesenchymal transition, and invasion of melanoma cells, while the overexpression of LINC00888 exerted opposite effect. Furthermore, we revealed that microRNA-126 (miR-126) was able to regulate LINC00888 expression and further influence the expression of CRK. Consistently, miR-126 inhibitor could rescue the expression of CRK in LINC00888-downregulated cells, while miR-126 mimics could reduce the CRK expression level in cells with the overexpression of LINC00888. Last, the animal experiment further demonstrated that the overexpression of LINC00888 enhanced the tumor development in vivo.
conclusionOur data showed that long-noncoding RNA LINC00888 functioned as an oncogene in melanoma tumorigenesis, it also regulated the cellular proliferation and invasion of melanoma via miR126/CRK signaling pathway and metastasis via miR-126/CRK signaling axis, which could be a promising molecular target for treating melanoma.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.