lactoferrin and Precursor-T-Cell-Lymphoblastic-Leukemia-Lymphoma

To explore the effects and possible mechanisms of decitabine on Molt4 in vitro.. Effects of decitabine on cells proliferation were detected by using CCK-8, the apoptosis by Annexin V-FITC, cell cycles by propidium iodide-FACS. Discrepancy genes were screened by RNA-seq technique. The CpG methylation of lactoferrin (LTF) gene in Molt4 cells were identified by Bisulfite sequencing PCR (BSP). The expression of LTF mRNA in Molt4 by RT-PCR and LTF protein expression were analyzed by Western blot.. Decitabine effectively inhibited proliferation and induced apoptosis for Molt4 cells by an time- and dose-dependent manners. Cell cycles were arrested at the G₀/G₁ phase. The promoter methylation degree of LTF gene in Molt4 cells was 72.3% before decitabine treatment and decreased to 45.0% after treatment with 0.50 μmol/L decitabine for 72 h. After the reduction of methylation, expression of its mRNA and protein increased, meanwhile caspase 3 and caspase 9 protein expression levels increased.. The demethylating drug decitabine can induce apoptosis, detain cell cycle at phase G₀/G₁, inhibit proliferation and up-regulate LTF gene expression in Molt4 cells. LTF may become a new target for acute T lymphoblastic leukemia.

Topics: Antimetabolites, Antineoplastic; Apoptosis; Azacitidine; Caspase 3; Cell Cycle; Cell Line, Tumor; Cell Proliferation; Decitabine; DNA Methylation; Humans; Lactoferrin; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma; Promoter Regions, Genetic