| Title |
LINC00888 promoted tumorigenicity of melanoma via miR-126/CRK signaling axis
|
|---|---|
| Published in |
OncoTargets and therapy, July 2018
|
| DOI | 10.2147/ott.s164711 |
| Pubmed ID | |
| Authors |
Wei Lu, Xiaohua Tao, Yibin Fan, Yi Tang, Xin Xu, Shasha Fan, Youming Huang, Yong Yu, Dan Luo |
| Abstract |
Melanoma 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. In 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. Elevated 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. Our 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. |
X Demographics
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Geographical breakdown
| Country | Count | As % |
|---|---|---|
| United States | 1 | 50% |
| Australia | 1 | 50% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 2 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 6 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 6 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Bachelor | 2 | 33% |
| Student > Ph. D. Student | 1 | 17% |
| Researcher | 1 | 17% |
| Student > Master | 1 | 17% |
| Unknown | 1 | 17% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 2 | 33% |
| Medicine and Dentistry | 2 | 33% |
| Engineering | 1 | 17% |
| Unknown | 1 | 17% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 15 August 2018.
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#19,954,338
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Outputs of similar age from OncoTargets and therapy
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