Galasso, M, Morrison, C, Minotti, L, Corra, F, Zerbinati, C, Agnoletto, C, Baldassari, F, Fassan, M, Bartolazzi, A, Di Leva, G 
ORCID: https://orcid.org/0000-0002-7656-510X, Nuovo, G, Vecchione, A, D'Atri, S, Alvino, E, Previati, M, Nickoloff, B, Croce, C and Volinia, S
2018,
'Loss of miR-204 expression is a key event in melanoma'
, Molecular Cancer, 17 (71)
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Abstract
Cutaneous melanoma (CM) is a malignancy with increasing occurrence. Its microRNA repertoire has been defined in a number studies, leading to candidates for biological and clinical relevance: miR-200a/b/c, miR-203, miR-205, miR-204, miR-211, miR-23b and miR-26a/b. Our work was aimed to validate the role of these candidate miRNAs in melanoma, using additional patients cohorts and in vitro cultures. miR-26a, miR-204 and miR-211 were more expressed in normal melanocytes, while miR-23b, miR-200b/c, miR-203 and miR-205 in epidermis and keratinocytes. None of the keratinocyte-related miRNAs was associated with any known mutation or with clinical covariates in melanoma.
On the other hand, the loss of miR-204 was enriched in melanomas with NRAS sole mutation (Fisher exact test, P = 0.001, Log Odds = 1.67), and less frequent than expected in those harbouring CDKN2A mutations (Fisher exact test, P = 0.001, Log Odds − 1.09). Additionally, miR-204 was associated with better prognosis in two independent melanoma cohorts and its exogenous expression led to growth impairment in melanoma cell lines. Thus, miR-204 represents a relevant mechanism in melanoma, with potential prognostic value and its loss seems to act in the CDKN2A pathway, in cooperation with NRAS.
| Item Type: | Article |
|---|---|
| Schools: | Schools > School of Environment and Life Sciences > Biomedical Research Centre |
| Journal or Publication Title: | Molecular Cancer |
| Publisher: | BioMed Central |
| ISSN: | 1476-4598 |
| Related URLs: | |
| Depositing User: | G Di Leva |
| Date Deposited: | 21 Mar 2018 13:07 |
| Last Modified: | 24 May 2019 11:45 |
| URI: | http://usir.salford.ac.uk/id/eprint/46305 |
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