Publication: A mutation in protein phosphatase
type 2A as a cause of melanoma progression
Authors
Ito, A. ; Koma, Y. ; Watabe, K.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The BL6 subline was derived from the F10
line, which was derived from the B16 mouse melanoma
cell line. BL6 cells are more invasive than F10 cells and
differ genetically from F10 cells by an alteration of the
gene encoding the B56? regulatory subunit of protein
phosphatase 2A (PP2A). This alteration results in the
transcription of mRNA encoding a truncated variant of
the B56?1 isoform (??1). ??1 is capable of targeting
PP2A to the specific subcellular sites but incapable of
promoting the dephosphorylation of specific substrates
that is normally mediated by the B56? subunitcontaining
PP2A holoenzyme. It thus appears that
activities of this type of holoenzymes decrease in cells
expressing ??1. Recently, we found two possible ways
how ??1 contributes to the enhanced metastatic potential
of BL6 cells. The two ways seemed far away from each
other: ??1 influenced both the nuclear and cytoplasmic
functions of the cell. In the cytoplasm, ??1 localized at
the Golgi complex and accelerated Golgi-mediated
vesicle transport. On the other hand, ??1 disturbed the
cell-cycle regulation. In response to g-irradiation, protein
levels of ??1 were markedly increased in BL6 cells.
Subsequently the integrity of cell-cycle checkpoint
became more aberrant in BL6 cells than that in F10
cells. These two actions of ??1 could results in the
enhancement of the malignant phenotypes of melanoma
cells, as discussed in this review.
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