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Sirt5 is dispensable for Braf V600E ‐mediated cutaneous melanoma development and growth in vivo
Author(s) -
Moon Hyeongsun,
Zhu Jerry,
White Andrew C.
Publication year - 2019
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.13845
Subject(s) - melanoma , cancer research , in vivo , knockout mouse , function (biology) , suppressor , mutation , biology , chemistry , cancer , microbiology and biotechnology , genetics , gene
Sirt5 is known to functionally regulate mitochondrial proteins by altering posttranslational modifications, including lysine desuccinylation. While roles for Sirt5 as either a tumor promoter or suppressor, or in chemoresistance, have been implicated in other cancers, the function of Sirt5 in cutaneous melanoma has not been well examined. Therefore, to determine whether Sirt5 is necessary for Braf V600E ‐mediated melanoma formation and/or disease progression, we crossed a genetically engineered murine melanoma model ( Tyr CreERT2 /+ ; Braf LSL ‐ V600E /+ ; Pten flox/flox ) to Sirt5 −/− knockout animals. In addition, we tested for synergism with a selective BRAF (V600E) inhibitor in Sirt5 −/− mouse melanoma cells. Taken together, this report demonstrates that, in these models, Sirt5 is dispensable for Braf V600E ‐mediated cutaneous melanoma formation and growth in vivo , and does not improve sensitivity to a selective BRAF inhibitor.