title: Expression profiling of choline and ethanolamine kinases in MCF7, HCT116 and HepG2 cells, and the transcriptional regulation by epigenetic modification.
abstract: The function of choline kinase (CK) and ethanolamine kinase (EK) is to catalyse the phosphorylation of choline and ethanolamine, respectively, in order to yield phosphocholine (PCho) and phosphoethanolamine (PEtn). A high expression level of PCho, due to elevated CK activity, has previously been associated with malignant transformation. In the present study, a quantitative polymerase chain reaction was performed to determine the mRNA expression profiles of ck and ek mRNA variants in MCF7 breast, HCT116 colon and HepG2 liver cancer cells. The ck and ek mRNA expression profiles showed that total ckα was expressed most abundantly in the HepG2 cells. The HCT116 cells exhibited the highest ckβ and ek1 mRNA expression levels, whereas the highest ek2α mRNA expression levels were detected in the MCF7 cells. The ckβ variant had higher mRNA expression levels, as compared with total ckα, in both the MCF7 and HCT116 cells. Relatively low ek1 mRNA expression levels were detected, as compared with ek2α in the MCF7 cells; however, this was not observed in the HCT116 and HepG2 cells. Notably, the mRNA expression levels of ckα2 were markedly low, as compared with ckα1, in all three cancer cell lines. The effects of epigenetic modification on ck and ek mRNA expression, by treatment of the cells with the histone deacetylase inhibitor trichostatin A (TSA), were also investigated. The results of the present study showed that the mRNA expression levels of ckα, ckβ and ek2α were affected by TSA. An increase >8-fold was observed in ek2α mRNA expression upon treatment with TSA, in a concentration- and time-dependent manner. In conclusion, the levels of ck and ek transcript variants in the three cancer cell lines were varied. The effects of TSA treatment on the mRNA expression levels of ck and ek imply that ck and ek mRNA expression may be regulated by epigenetic modification.
authors.affiliation: School of Health Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan 16150, Malaysia.
authors.forename: Chua Siang
authors.initials: CS
authors.lastname: Ling
authors.affiliation: Institute for Research in Molecular Medicine, Universiti Sains Malaysia, Penang 11800, Malaysia.
authors.forename: Khoo Boon
authors.initials: KB
authors.lastname: Yin
authors.affiliation: School of Health Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan 16150, Malaysia.
authors.forename: See Too Wei
authors.initials: ST
authors.lastname: Cun
authors.affiliation: School of Health Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan 16150, Malaysia.
authors.forename: Few Ling
authors.initials: FL
authors.lastname: Ling
mesh_terms: D045744:Cell Line, Tumor; D002797:Choline Kinase / Q000235:genetics*; D044127:Epigenesis, Genetic; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D056945:Hep G2 Cells; D006801:Humans; D061986:MCF-7 Cells; D017853:Phosphotransferases (Alcohol Group Acceptor) / Q000235:genetics*; D014158:Transcription, Genetic
chemical_list: D017853:Phosphotransferases (Alcohol Group Acceptor); D002797:Choline Kinase; C020125:ethanolamine kinase