Abstract
5-Hydroxymethylcytosine (5hmC) is lost in multiple human cancers, including colorectal cancer (CRC). Decreased ten-eleven translocation 1 (TET1) messenger RNA (mRNA), but not other two TET family members, has been observed in the colorectal cancer and is crucial for colorectal cancer initiation. Here, we show that nuclear localization of TET2 was lost in a significant portion of CRC tissues, in association with metastasis. In CRC cells, nuclear expression of TET2 were absent but not TET3. Nuclear export inhibitor can increase the 5hmC level in CRC cells, probably through regulating TET2. Our results indicate a new mechanism of TET2 dysregulation in colorectal cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/s13148-016-0176-7) contains supplementary material, which is available to authorized users.
Highlights
5-Hydroxymethylcytosine (5hmC) is lost in multiple human cancers, including colorectal cancer (CRC)
F Neri et al reported the downregulation of ten-eleven translocation 1 (TET1) messenger RNA expression level, but not other two ten-eleven translocation (TET) family members, in colon cancer and showed that decreased TET1 mRNA was crucial for colon cancer initiation and TET1 functioned as a tumor suppressor by inhibiting the WNT pathway [1]
It was reported that the reduced levels of 5hmC in colorectal cancers is not correlated with TET mRNA levels [3], which indicates that dysregulation of TET protein could play a vital role in colorectal cancer
Summary
5-Hydroxymethylcytosine (5hmC) is lost in multiple human cancers, including colorectal cancer (CRC). Another group observed the decreased mRNA level of all TET family members in the colorectal cancer [2]. We analyzed both the mRNA and protein level of the TET family members in our colorectal cancer specimens.
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