m6A-centered Disease Response Information
General Information of the Disease (ID: M6ADIS0003)
| Name |
Mature T-cell lymphoma
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|---|---|---|---|---|---|
| ICD |
ICD-11: 2A90
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Full List of Target Gene(s) of This m6A-centered Disease Response
Cyclin-dependent kinase inhibitor 2A (CDKN2A)
| In total 2 item(s) under this target gene | ||||
| Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene | [1] | |||
| Response Summary | The decline in METTL3 levels was responsible for CTCL cell proliferation and migration,Cyclin-dependent kinase inhibitor 2A (CDKN2A) was a key regulator during this process in vitro and in vivo, and insufficient methylation modification blocked the interaction between CDKN2A and m6A reader IGF2BP2, resulting in mRNA degradation. | |||
| Responsed Disease | Mature T-cell lymphoma [ICD-11: 2A90] | |||
| Target Regulator | Methyltransferase-like 3 (METTL3) | WRITER | ||
| Target Regulation | Up regulation | |||
| Cell Process | Cell proliferation | |||
| Cell migration | ||||
| Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene | [1] | |||
| Response Summary | The decline in METTL3 levels was responsible for CTCL cell proliferation and migration,Cyclin-dependent kinase inhibitor 2A (CDKN2A) was a key regulator during this process in vitro and in vivo, and insufficient methylation modification blocked the interaction between CDKN2A and m6A reader IGF2BP2, resulting in mRNA degradation. | |||
| Responsed Disease | Mature T-cell lymphoma [ICD-11: 2A90] | |||
| Target Regulator | Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) | READER | ||
| Target Regulation | Up regulation | |||
| Cell Process | Cell proliferation | |||
| Cell migration | ||||
Ubiquitin carboxyl-terminal hydrolase 1 (USP1)
| In total 2 item(s) under this target gene | ||||
| Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene | [2] | |||
| Response Summary | ALKBH5 and Ubiquitin carboxyl-terminal hydrolase 1 (USP1) were upregulated in T-cell acute lymphoblastic leukemia, and ALKBH5-mediated m6A modification increased USP1 and Aurora B expression. Silencing USP1 increased CEM-C1 cell sensitivity to dexamethasone, reduced cell invasion, promoted cell apoptosis, and ameliorated glucocorticoid receptor (GR) expression. | |||
| Responsed Disease | Mature T-cell lymphoma [ICD-11: 2A90] | |||
| Responsed Drug | dexamethasone | Approved | ||
| Target Regulator | RNA demethylase ALKBH5 (ALKBH5) | ERASER | ||
| Target Regulation | Up regulation | |||
| Cell Process | Cell apoptosis | |||
| In-vitro Model | CEM/C1 | T acute lymphoblastic leukemia | Homo sapiens | CVCL_3496 |
| CCRF-CEM C7 | T acute lymphoblastic leukemia | Homo sapiens | CVCL_6825 | |
| HEK293T | Normal | Homo sapiens | CVCL_0063 | |
| In-vivo Model | Adult male C57BL/6J mice (weighting 18-25 g) were obtained from Laboratory Animal Center, Zhengzhou University. Mice were subcutaneously injected with 1 × 107 CEM-C1 cells for tumorigenesis and randomly divided into four group: control group; control + Dex; sh-RNA + Dex; sh-USP1 + Dex. Mice treatment with Dex were intraperitoneally injected with 8 mg/kg Dex every day for 10 consecutive days after tumor growth and mice treatment with sh-RNA or sh-USP1 were injected intravenously with 2 mg/Kg sh-RNA or USP1 sh-RNA. The control group of mice were injected with the same volume of normal saline. After the treatment of each group, the mice were housed and fed in a room with an ambient temperature of 25℃, and the survival time, weight of the mice, and tumor weight were recorded. When rats were sacrificed, tissues were harvested for Western blot analysis. | |||
| Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene | [2] | |||
| Response Summary | ALKBH5 and Ubiquitin carboxyl-terminal hydrolase 1 (USP1) were upregulated in T-cell acute lymphoblastic leukemia, and ALKBH5-mediated m6A modification increased USP1 and Aurora B expression. Silencing USP1 increased CEM-C1 cell sensitivity to dexamethasone, reduced cell invasion, promoted cell apoptosis, and ameliorated glucocorticoid receptor (GR) expression. | |||
| Responsed Disease | Mature T-cell lymphoma [ICD-11: 2A90] | |||
| Responsed Drug | Glucocorticoid | Investigative | ||
| Target Regulator | RNA demethylase ALKBH5 (ALKBH5) | ERASER | ||
| Target Regulation | Up regulation | |||
| Cell Process | Cell apoptosis | |||
| In-vitro Model | CEM/C1 | T acute lymphoblastic leukemia | Homo sapiens | CVCL_3496 |
| CCRF-CEM C7 | T acute lymphoblastic leukemia | Homo sapiens | CVCL_6825 | |
| HEK293T | Normal | Homo sapiens | CVCL_0063 | |
| In-vivo Model | Adult male C57BL/6J mice (weighting 18-25 g) were obtained from Laboratory Animal Center, Zhengzhou University. Mice were subcutaneously injected with 1 × 107 CEM-C1 cells for tumorigenesis and randomly divided into four group: control group; control + Dex; sh-RNA + Dex; sh-USP1 + Dex. Mice treatment with Dex were intraperitoneally injected with 8 mg/kg Dex every day for 10 consecutive days after tumor growth and mice treatment with sh-RNA or sh-USP1 were injected intravenously with 2 mg/Kg sh-RNA or USP1 sh-RNA. The control group of mice were injected with the same volume of normal saline. After the treatment of each group, the mice were housed and fed in a room with an ambient temperature of 25℃, and the survival time, weight of the mice, and tumor weight were recorded. When rats were sacrificed, tissues were harvested for Western blot analysis. | |||
References