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2 results on '"Metallothionein III"'

1. Metallothionein III (MT3) is a putative tumor suppressor gene that is frequently inactivated in pediatric acute myeloid leukemia by promoter hypermethylation.

Author

Yan-Fang Tao, Li-Xiao Xu, Jun Lu, Lan Cao, Zhi-Heng Li, Shao-Yan Hu, Na-Na Wang, Xiao-Juan Du, Li-Chao Sun, Wen-Li Zhao, Pei-Fang Xiao, Fang Fang, Yan-Hong Li, Gang Li, He Zhao, Yi-Ping Li, Yun-Yun Xu, Jian Ni, Jian Wang, and Xing Feng

Subjects
*METALLOTHIONEIN, *ACUTE myeloid leukemia, *TUMOR suppressor genes, *LEUKEMIA in children, *METHYLATION
Abstract

Background Acute myeloid leukemia (AML) is the second most common form of leukemia in children. Aberrant DNA methylation patterns are a characteristic feature in various tumors, including AML. Metallothionein III (MT3) is a tumor suppresser reported to show promoter hypermethylated in various cancers. However, the expression and molecular function of MT3 in pediatric AML is unclear. Methods Eleven human leukemia cell lines and 41 pediatric AML samples and 20 NBM/ITP (Norma bone marrow / Idiopathic thrombocytopenic purpura) control samples were analyzed. Transcription levels of MT3 were evaluated by semi-quantitative and real-time PCR. MT3 methylation status was determined by methylation specific PCR (MSP) and bisulfite genomic sequencing (BSG). The molecular mechanism of MT3 was investigated by apoptosis assays and PCR array analysis. Results The MT3 promoter was hypermethylated in leukemia cell lines. More CpG's methylated of MT3 was observed 39.0% pediatric AML samples compared to 10.0% NBM controls. Transcription of MT3 was also significantly decreased in AML samples compared to NBM/ITP controls (P < 0.001); patients with methylated MT3 exhibited lower levels of MT3 expression compared to those with unmethylated MT3 (P = 0.049). After transfection with MT3 lentivirus, proliferation was significantly inhibited in AML cells in a dose-dependent manner (P < 0.05). Annexin V assay showed that apoptosis was significantly upregulated MT3-overexpressing AML cells compared to controls. Real-time PCR array analysis revealed 34 dysregulated genes that may be implicated in MT3 overexpression and apoptosis in AML, including FOXO1. Conclusion MT3 may be a putative tumor suppressor gene in pediatric AML. Epigenetic inactivation of MT3 via promoter hypermethylation was observed in both AML cell lines and pediatric AML samples. Overexpression of MT3 may inhibit proliferation and induce apoptosis in AML cells. FOXO1 was dysregulated in MT3-overexpressing cells, offering an insight into the mechanism of MT3-induced apoptosis. However, further research is required to determine the underlying molecular details. [ABSTRACT FROM AUTHOR]

Published
2014
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2. Metallothionein III (MT3) is a putative tumor suppressor gene that is frequently inactivated in pediatric acute myeloid leukemia by promoter hypermethylation

Author

Shaoyan Hu, Yanhong Li, Jun Lu, Yunyun Xu, Wenli Zhao, Peifang Xiao, Jian Wang, Lan Cao, Yi-Ping Li, Yan-Fang Tao, He Zhao, Li-Xiao Xu, Fang Fang, Jian Pan, Na-Na Wang, Zhi-Heng Li, Lichao Sun, Xiao-Juan Du, Xing Feng, Gang Li, and Jian Ni

Subjects
Male, Myeloid, Tumor suppressor gene, Adolescent, Bisulfite sequencing, Nerve Tissue Proteins, Biology, Polymerase Chain Reaction, Methylation, General Biochemistry, Genetics and Molecular Biology, Pediatric acute myeloid leukemia, hemic and lymphatic diseases, Cell Line, Tumor, medicine, Humans, Genes, Tumor Suppressor, Epigenetics, Child, Promoter Regions, Genetic, DNA Primers, Medicine(all), Base Sequence, Biochemistry, Genetics and Molecular Biology(all), Research, Myeloid leukemia, Infant, Tumor suppressor, General Medicine, DNA Methylation, medicine.disease, Metallothionein 3, Leukemia, Leukemia, Myeloid, Acute, Metallothionein III, medicine.anatomical_structure, Child, Preschool, DNA methylation, Cancer research, Female
Abstract

Background: Acute myeloid leukemia (AML) is the second most common form of leukemia in children. Aberrant DNA methylation patterns are a characteristic feature in various tumors, including AML. Metallothionein III (MT3) is a tumor suppresser reported to show promoter hypermethylated in various cancers. However, the expression and molecular function of MT3 in pediatric AML is unclear. Methods: Eleven human leukemia cell lines and 41 pediatric AML samples and 20 NBM/ITP (Norma bone marrow/ Idiopathic thrombocytopenic purpura) control samples were analyzed. Transcription levels of MT3 were evaluated by semi-quantitative and real-time PCR. MT3 methylation status was determined by methylation specific PCR (MSP) and bisulfite genomic sequencing (BSG). The molecular mechanism of MT3 was investigated by apoptosis assays and PCR array analysis. Results: The MT3 promoter was hypermethylated in leukemia cell lines. More CpG’s methylated of MT3 was observed 39.0% pediatric AML samples compared to 10.0% NBM controls. Transcription of MT3 was also significantly decreased in AML samples compared to NBM/ITP controls (P< 0.001); patients with methylated MT3 exhibited lower levels of MT3 expression compared to those with unmethylated MT3 (P = 0.049). After transfection with MT3 lentivirus, proliferation was significantly inhibited in AML cells in a dose-dependent manner (P< 0.05). Annexin V assay showed that apoptosis was significantly upregulated MT3-overexpressing AML cells compared to controls. Real-time PCR array analysis revealed 34 dysregulated genes that may be implicated in MT3 overexpression and apoptosis in AML, including FOXO1. Conclusion: MT3 may be a putative tumor suppressor gene in pediatric AML. Epigenetic inactivation of MT3 via promoter hypermethylation was observed in both AML cell lines and pediatric AML samples. Overexpression of MT3 may inhibit proliferation and induce apoptosis in AML cells. FOXO1 was dysregulated in MT3-overexpressing cells, offering an insight into the mechanism of MT3-induced apoptosis. However, further research is required to determine the underlying molecular details.

Published
2014

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