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Haspin is a survival factor for H3T3 phosphorylation and survivin recruitment in malignancy of colorectal cancer
Author(s) -
Lee TsaiChia,
Chang YunHsuan,
Yu TzuWei,
Shen TzuKeng,
Tsai MingChang,
Huang ChiChou,
Yang TzuWei,
Lin ChunChe,
Chiou GuangYuh,
Jong YuhJyh,
Chao JuiI
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb180
Subject(s) - survivin , colorectal cancer , cancer research , kinase , phosphorylation , biology , cancer , cancer cell , histone h3 , histone , microbiology and biotechnology , biochemistry , genetics , gene
Colorectal cancer (CRC) is one of the leading causes of cancer‐related morbidity and mortality in the world. Haspin is a histone H3 kinase that mediates the phosphorylation of H3 at threonine 3 (p‐H3T3), which recruits chromosomal passenger complex (CPC) and promotes cell division. However, the precise role of Haspin in CRC is still unclear. Here we show that overexpression of Haspin increased the protein levels of H3T3 and Survivin in CRC cells. Moreover, the Haspin and p‐H3T3 protein levels were highly expressed in CRC tumor tissues but not in normal tissues from clinical CRC patients. Interestingly, we found that Haspin proteins were inhibited but conversely elicited the stemness protein expression of CD133 in CRC tissues using 3‐D tissue culture condition. The similar results were verified by immunofluorescence staining and confocal microscopy. We suggest that Haspin exhibits a crucial role in the regulation of malignant and cancer stemness of CRC; however, the precise mechanism should be further investigated.