Abstract
The incidence of melanoma, the most aggressive and life-threatening form of skin cancer, has significantly risen over recent decades. Therefore, it is essential to identify the mechanisms that underlie melanoma tumorigenesis and metastasis and to explore novel and effective melanoma treatment strategies. Accumulating evidence s uggests that aberrantly expressed long noncoding RNAs (lncRNAs) have vital functions in multiple cancers. However, lncRNA functions in melanoma tumorigenesis and metastasis remain unclear. In this study, we investigated lncRNA and messenger RNA (mRNA) expression profiles in primary melanomas, metastatic melanomas and normal skin samples from the Gene Expression Omnibus database. We used GSE15605 as the training set (n = 74) and GSE7553 as the validation set (n = 58). In three comparisons (primary melanoma versus normal skin, metastatic melanoma versus normal skin, and metastatic melanoma versus primary melanoma), 178, 295 and 48 lncRNAs and 847, 1758, and 295 mRNAs were aberrantly expressed, respectively. We performed Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses to examine the differentially expressed mRNAs, and potential core lncRNAs were predicted by lncRNA-mRNA co-expression networks. Based on our results, 15 lncRNAs and 144 mRNAs were significantly associated with melanoma tumorigenesis and metastasis. A subsequent analysis suggested a critical role for a five-lncRNA signature during melanoma tumorigenesis and metastasis. Low expression of U47924.27 was significantly associated with decreased survival of patients with melanoma. To the best of our knowledge, this study is the first to explore the expression patterns of lncRNAs and mRNAs during melanoma tumorigenesis and metastasis by re-annotating microarray data from the Gene Expression Omnibus (GEO) microarray dataset. These findings reveal potential roles for lncRNAs during melanoma tumorigenesis and metastasis and provide a rich candidate reservoir for future studies.
Highlights
The worldwide incidence of melanoma, the most aggressive form of skin cancer, has rapidly increased in recent decades
Since we focused on identifying Long noncoding RNAs (lncRNAs) that are abnormally expressed during melanoma tumorigenesis and metastasis, only SPRY4-IT1 was included in our final lncRNA signature
We primarily focused our study on the value of bioinformatics-based analyses for discovering novel or important lncRNAs and messenger RNA (mRNA) expressed during melanoma tumorigenesis and metastasis
Summary
The worldwide incidence of melanoma, the most aggressive form of skin cancer, has rapidly increased in recent decades. Primary melanoma (PM) is curable by surgery. If it is not detected early and surgically removed, melanoma is highly likely to metastasize. Identification of the mechanisms driving both tumorigenesis and metastasis and the development of novel and effective melanoma treatment strategies are urgently needed. The first functional lncRNA, XIST, was discovered in the early 1990s; XIST inactivates gene expression from the X-chromosome by dosage equalization [4, 5]. Multiple reports have shown that lncRNAs regulate complex and diverse functions, including embryonic stem cell pluripotency [6], epigenetic gene regulation [7], the DNA damage response [8], and chromatin remodeling [9]. LncRNAs participate in wide-ranging cellular processes, including cell cycle, proliferation, apoptosis, and invasion [10]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
