INPP4B: the new kid on the PI3K block.
INPP4B: the new kid on the PI3K block.
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DOI：
10.18632/oncotarget.260
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发表时间：
2011-04
期刊：
影响因子：
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通讯作者：
Ittmann MM
中科院分区：
文献类型：
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作者：
Agoulnik IU;Hodgson MC;Bowden WA;Ittmann MM
磷脂酰肌醇信号转导失调发生在许多癌症和其他疾病中。脂质和蛋白磷酸酶，PTEN（染色体10上的磷酸酶和张力蛋白同源蛋白），是已知的肿瘤抑制因子，其功能在各种恶性肿瘤中由于编码区中的突变或基因组缺失而经常丧失。最近，另一种脂质磷酸酶，肌醇多磷酸4-磷酸酶II型（INPP 4 B），已成为前列腺癌，乳腺癌和卵巢癌的潜在肿瘤抑制因子，并可能在白血病。我们将回顾其结构和功能，与雄激素受体信号传导的串扰，以及INPP 4 B表达的调节，以及现有的关于其在癌症中的作用的数据。
Dysregulation of phosphatidyl inositol signaling occurs in many cancers and other disorders. The lipid and protein phosphatase, PTEN (Phosphatase and Tensin homology protein on chromosome 10), is a known tumor suppressor whose function is frequently lost in various malignancies due to mutations in the coding region or genomic deletions. Recently, another lipid phosphatase, Inositol Polyphosphate 4-phosphatase type II (INPP4B), has emerged as a potential tumor suppressor in prostate, breast, and ovarian cancers and possibly in leukemia. We will review its structure and function, crosstalk with androgen receptor signaling, and regulation of INPP4B expression, as well as existing data about its role in cancer.