m6A Target Gene Information
General Information of the m6A Target Gene (ID: M6ATAR00017)
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
hsa-miR-143-3p
can be regulated by the following regulator(s), and cause disease/drug response(s). You can browse detail information of regulator(s) or disease/drug response(s).
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Methyltransferase-like 3 (METTL3) [WRITER]
| In total 2 item(s) under this regulator | ||||
| Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [1] | |||
| Response Summary | m6A methyltransferase Mettl3 can increase the splicing of precursor hsa-miR-143-3p to facilitate its biogenesis. The miR-143-3p/VASH1 axis in BM of lung cancers and suggests their critical roles in lung cancer pathogenesis. | |||
| Target Regulation | Down regulation | |||
| Responsed Disease | Lung cancer | ICD-11: 2C25 | ||
| Pathway Response | RNA degradation | hsa03018 | ||
| Cell Process | RNA splicing | |||
| In-vitro Model | A-549 | Lung adenocarcinoma | Homo sapiens | CVCL_0023 |
| NCI-H1975 | Lung adenocarcinoma | Homo sapiens | CVCL_1511 | |
| In-vivo Model | For subcutaneous transplanted model, control and miR-143-3p stable A549 cells (5 × 106 per mouse, n = 5 for each group) were diluted in 200 uL PBS + 200 uL Matrigel (BD Biosciences) and subcutaneously injected into immunodeficient mice to investigate tumor growth. | |||
| Experiment 2 Reporting the m6A Methylation Regulator of This Target Gene | [2] | |||
| Response Summary | METTL3 promoted DGCR8 binding to pri-miR-143-3p through m6A modification, thus enhancing hsa-miR-143-3p expression to inhibit PRKCE transcription and further aggravating cardiomyocyte pyroptosis and MI/R injury. | |||
| Target Regulation | Up regulation | |||
| Responsed Disease | Ischemic heart disease | ICD-11: BA40-BA6Z | ||
| Cell Process | Pyroptosis | |||
| In-vitro Model | H9c2(2-1) | Normal | Rattus norvegicus | CVCL_0286 |
| In-vivo Model | The thoracic cavity of rats was exposed, and the left anterior descending coronary artery was ligated with a 6-0 silk thread. Successfully surgical MI could be observed, with myocardium color fading and pulse weakening. After 30 min of ischemia, the blood flow was restored by releasing the slipknot, and then 120-min perfusion was performed. Afterward, the thoracic cavity of rats was sutured. The rats were assigned into 4 groups, with 12 rats in each group. Lentivirus packaged short hairpin (sh)-negative control (NC) and sh-METTL3 (GenePharma, Shanghai, China) were injected into the rats via tail vein 24 h before operation. The titer of lentivirus was 1?×?109 TU/mL, and the injection rate was 0.2 ul/min for 10 min. Blood samples were collected 24 h after reperfusion. | |||
Lung cancer [ICD-11: 2C25]
| In total 1 item(s) under this disease | ||||
| Experiment 1 Reporting the m6A-centered Disease Response | [1] | |||
| Response Summary | m6A methyltransferase Mettl3 can increase the splicing of precursor hsa-miR-143-3p to facilitate its biogenesis. The miR-143-3p/VASH1 axis in BM of lung cancers and suggests their critical roles in lung cancer pathogenesis. | |||
| Responsed Disease | Lung cancer [ICD-11: 2C25] | |||
| Target Regulator | Methyltransferase-like 3 (METTL3) | WRITER | ||
| Target Regulation | Down regulation | |||
| Pathway Response | RNA degradation | hsa03018 | ||
| Cell Process | RNA splicing | |||
| In-vitro Model | A-549 | Lung adenocarcinoma | Homo sapiens | CVCL_0023 |
| NCI-H1975 | Lung adenocarcinoma | Homo sapiens | CVCL_1511 | |
| In-vivo Model | For subcutaneous transplanted model, control and miR-143-3p stable A549 cells (5 × 106 per mouse, n = 5 for each group) were diluted in 200 uL PBS + 200 uL Matrigel (BD Biosciences) and subcutaneously injected into immunodeficient mice to investigate tumor growth. | |||
Ischemic heart disease [ICD-11: BA40-BA6Z]
| In total 1 item(s) under this disease | ||||
| Experiment 1 Reporting the m6A-centered Disease Response | [2] | |||
| Response Summary | METTL3 promoted DGCR8 binding to pri-miR-143-3p through m6A modification, thus enhancing hsa-miR-143-3p expression to inhibit PRKCE transcription and further aggravating cardiomyocyte pyroptosis and MI/R injury. | |||
| Responsed Disease | Ischemic heart disease [ICD-11: BA40-BA6Z] | |||
| Target Regulator | Methyltransferase-like 3 (METTL3) | WRITER | ||
| Target Regulation | Up regulation | |||
| Cell Process | Pyroptosis | |||
| In-vitro Model | H9c2(2-1) | Normal | Rattus norvegicus | CVCL_0286 |
| In-vivo Model | The thoracic cavity of rats was exposed, and the left anterior descending coronary artery was ligated with a 6-0 silk thread. Successfully surgical MI could be observed, with myocardium color fading and pulse weakening. After 30 min of ischemia, the blood flow was restored by releasing the slipknot, and then 120-min perfusion was performed. Afterward, the thoracic cavity of rats was sutured. The rats were assigned into 4 groups, with 12 rats in each group. Lentivirus packaged short hairpin (sh)-negative control (NC) and sh-METTL3 (GenePharma, Shanghai, China) were injected into the rats via tail vein 24 h before operation. The titer of lentivirus was 1?×?109 TU/mL, and the injection rate was 0.2 ul/min for 10 min. Blood samples were collected 24 h after reperfusion. | |||
References