Abstract

Significant advances have been made in the treatment of melanoma by targeting key cellular pathways, but additional targets are needed as many patients do not respond or relapse with resistant disease. MicroRNA-155 (MiR-155) has previously been shown to regulate melanoma cell growth and acts as a tumor suppressor. We tested a clinical population of melanoma tumors for miR-155 expression, and find that expression is low in most patients, although not predictive of outcome. We identified the protein kinase WEE1 as a novel target of miR-155. A mouse model of experimental metastasis finds that both increased expression of miR-155 and silencing of WEE1 lead to decreased metastases. Loss of miR-155 and increased expression of WEE1 may contribute to the metastatic phenotype in patients with melanoma.

Original languageEnglish (US)
Pages (from-to)216-219
Number of pages4
JournalMelanoma Research
Volume29
Issue number2
DOIs
StatePublished - Apr 1 2019

Fingerprint

Melanoma
Up-Regulation
Neoplasm Metastasis
MicroRNAs
Protein Kinases
Neoplasms
Theoretical Models
Phenotype
Recurrence
Growth
Population
Therapeutics

All Science Journal Classification (ASJC) codes

  • Oncology
  • Dermatology
  • Cancer Research

Cite this

Disano, Julie A. ; Huffnagle, Ian ; Gowda, Raghavendra ; Spiegelman, Vladimir ; Robertson, Gavin ; Pameijer, Colette R. / Loss of miR-155 upregulates WEE1 in metastatic melanoma. In: Melanoma Research. 2019 ; Vol. 29, No. 2. pp. 216-219.
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abstract = "Significant advances have been made in the treatment of melanoma by targeting key cellular pathways, but additional targets are needed as many patients do not respond or relapse with resistant disease. MicroRNA-155 (MiR-155) has previously been shown to regulate melanoma cell growth and acts as a tumor suppressor. We tested a clinical population of melanoma tumors for miR-155 expression, and find that expression is low in most patients, although not predictive of outcome. We identified the protein kinase WEE1 as a novel target of miR-155. A mouse model of experimental metastasis finds that both increased expression of miR-155 and silencing of WEE1 lead to decreased metastases. Loss of miR-155 and increased expression of WEE1 may contribute to the metastatic phenotype in patients with melanoma.",
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Loss of miR-155 upregulates WEE1 in metastatic melanoma. / Disano, Julie A.; Huffnagle, Ian; Gowda, Raghavendra; Spiegelman, Vladimir; Robertson, Gavin; Pameijer, Colette R.

In: Melanoma Research, Vol. 29, No. 2, 01.04.2019, p. 216-219.

Research output: Contribution to journalArticle

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T1 - Loss of miR-155 upregulates WEE1 in metastatic melanoma

AU - Disano, Julie A.

AU - Huffnagle, Ian

AU - Gowda, Raghavendra

AU - Spiegelman, Vladimir

AU - Robertson, Gavin

AU - Pameijer, Colette R.

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AB - Significant advances have been made in the treatment of melanoma by targeting key cellular pathways, but additional targets are needed as many patients do not respond or relapse with resistant disease. MicroRNA-155 (MiR-155) has previously been shown to regulate melanoma cell growth and acts as a tumor suppressor. We tested a clinical population of melanoma tumors for miR-155 expression, and find that expression is low in most patients, although not predictive of outcome. We identified the protein kinase WEE1 as a novel target of miR-155. A mouse model of experimental metastasis finds that both increased expression of miR-155 and silencing of WEE1 lead to decreased metastases. Loss of miR-155 and increased expression of WEE1 may contribute to the metastatic phenotype in patients with melanoma.

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