Nuclear PTEN levels and G2 progression in melanoma cells.
Nuclear PTEN levels and G2 progression in melanoma cells.
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DOI：
10.1097/cmr.0b013e32832ccd6e
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发表时间：
2009-08
影响因子：
2.2
通讯作者：
Eng C
中科院分区：
文献类型：
--
作者：
Jacob AI;Romigh T;Waite KA;Eng C
磷酸酶和张力蛋白同源物（PTEN）部分地通过负调节众所周知的磷脂酰肌醇-3-激酶/AKT信号传导途径来发挥其功能。以前的组织学研究表明，PTEN的核/胞质区室化的改变可能在黑色素瘤的发展和进展中起作用。在这项研究中，我们研究了黑色素瘤细胞系中PTEN的核/质区室化及其与细胞周期的相关性。使用经典的细胞生物学技术在黑素瘤细胞系中进行研究。与乳腺癌细胞系相反，我们发现核PTEN水平的增加与G2而不是G1阻滞相关。在WM 164和SKmel 28细胞中，PTEN蛋白的过表达没有显著增加G2期细胞的数量。与PTEN下调的细胞相比，过表达PTEN的细胞中CDC 2磷酸化水平的差异表明PTEN在G2检查点调节中有一定的参与。这些数据表明，虽然核PTEN水平与G2期相关，但PTEN在调节G2/M期阻滞中的作用并不受限制。此外，由核PTEN调节的特定细胞周期时相是细胞类型依赖性的。总而言之，我们的观察表明，在黑色素瘤中，核PTEN可能通过调节CDC 2参与G2进展，这为研究开辟了新的竞技场。
The phosphatase and tensin homolog (PTEN) exerts its function, in part, by negatively regulating the well-known phosphatidylinositol-3-kinase/AKT signaling pathway. Previous histological work has suggested that alterations in the nuclear/cytoplasmic compartmentalization of PTEN may play a role in the development and progression of melanoma. In this study, we examined the nuclear/cytoplasmic compartmentalization of PTEN in melanoma cell lines and its correlation with the cell cycle. Studies were performed in melanoma cells lines using classic cell biological techniques. In contrast to breast cancer cell lines, we found that increased levels of nuclear PTEN levels correlate with G2 rather than with G1 arrest. In WM164 and SKmel28 cells, overexpression of PTEN protein did not significantly increase the number of cells in the G2 phase. Differential CDC2 phosphorylation levels in cells that overexpressed PTEN compared with those where PTEN was downregulated suggest some involvement of PTEN in G2 checkpoint regulation. The data suggest that although nuclear PTEN levels correlate with the G2 phase, the role of PTEN in modulating G2/M arrest is not limiting. Further, the specific cell cycle phase regulated by nuclear PTEN is cell-type dependent. Taken together, our observations suggest that in melanoma, nuclear PTEN is involved in G2 progression possibly through the modulation of CDC2, opening up a new arena for investigation.