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Overview
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Background
INH6 is a potent inhibitor of Hec1/Nek2 [1].
Hec1 is an oncogene that involved in spindle checkpoint signaling and is overexpressed in many human cancers. Nek2 is a serine/threonine-protein kinase that phosphorylates Hec1, which is critical for its mitotic function and cell survival [1].
INH6 is a potent Hec1/Nek2 inhibitor. INH6 inhibited Hec1/Nek2 function through protein degradation that led to chromosome mis-segregation and cell death. In MDA-MB468 and MDA-MB231 human breast cancer cell lines, HeLa human cervical cancer line and K562 human erythromyeloblastoid leukemia cell line, INH6 exhibited significantly anti-proliferation activities with IC50 values of 2.1, 1.7, 2.4 and 2.5 µM, respectively. In HeLa cell extract, INH6-conjugated matrix selectively co-precipitated with cellular Hec1, which suggested that INH6 bound to cellular Hec1. In Hela cells, INH6 (6.25 µM) reduced Nek2 by 50% at 8-11 h. In addition, INH6 slightly reduced Hec1 over time. Also, INH6 increased mitotic population with multipolar spindle configurations. In HeLa cells expressing the chromosome marker protein H2B-GFP, INH6 increased chromosome misalignment. In HeLa cells, INH6 exhibited progressive morphological changes of dying cells and induced apoptosis by 20% [1].
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