m6A Target Gene Information
General Information of the m6A Target Gene (ID: M6ATAR00335)
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
MMP9
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]
Representative RNA-seq result indicating the expression of this target gene regulated by METTL3 | ||
Cell Line | LX2 cell line | Homo sapiens |
Treatment: shMETTL3 LX2 cells
Control: shLuc LX2 cells
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GSE207909 | |
Regulation |
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logFC: 2.14E+00 p-value: 4.12E-24 |
More Results | Click to View More RNA-seq Results |
In total 2 item(s) under this regulator | ||||
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [1] | |||
Response Summary | METTL3-mediated formation of EV miR-93, facilitated by m6A, is implicated in the aberrant cross-talk of epithelium-macrophages, indicating that this process is involved in the smoking-related emphysema. EV miR-93 was used as a novel risk biomarker for CS-induced emphysema. MiR-93 activated the JNK pathway by targeting dual-specificity phosphatase 2 (DUSP2), which elevated the levels of Matrix metalloproteinase-9 (MMP9) and matrix metalloproteinase 12 (MMP12) and induced elastin degradation, leading to emphysema. | |||
Target Regulation | Down regulation | |||
Responsed Disease | Emphysema | ICD-11: CA21 | ||
Pathway Response | MAPK signaling pathway | hsa04010 | ||
Experiment 2 Reporting the m6A Methylation Regulator of This Target Gene | [2] | |||
Response Summary | METTL3 knockdown suppressed interleukin (IL)-6, matrix metalloproteinase (MMP)-3, and Matrix metalloproteinase-9 (MMP9) levels in human RA-FLSs and rat AIA-FLSs. | |||
Target Regulation | Up regulation | |||
Responsed Disease | Rheumatoid arthritis | ICD-11: FA20 | ||
Cell Process | Inflammatory response | |||
In-vitro Model | FLS (Rat fibroblast synovial cell line) | |||
In-vivo Model | To establish the adjuvant-induced arthritis (AIA) model, the rats were given complete Freund's adjuvant (CFA; Chondrex, Inc.) on the left paw of 0.1 ml per 100 g of body weight. Additionally, the rats were injected with normal saline to create the negative control (NC) group. | |||
E3 ubiquitin-protein ligase Hakai (CBLL1) [WRITER]
In total 1 item(s) under this regulator | ||||
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [3] | |||
Response Summary | CBLL1 was frequently upregulated in non-small lung cancer (NSCLC) tissues compared to the adjacent nontumor tissues. CBLL1 knockdown inhibited cell invasion via increased E-cadherin protein expression, and decreased expression of MMP2 and Matrix metalloproteinase-9 (MMP9) in NSCLC cell lines. | |||
Responsed Disease | Non-small-cell lung carcinoma | ICD-11: 2C25.Y | ||
In-vitro Model | A-549 | Lung adenocarcinoma | Homo sapiens | CVCL_0023 |
NCI-H1299 | Lung large cell carcinoma | Homo sapiens | CVCL_0060 | |
SK-MES-1 | Lung squamous cell carcinoma | Homo sapiens | CVCL_0630 | |
Lung cancer [ICD-11: 2C25]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the m6A-centered Disease Response | [3] | |||
Response Summary | CBLL1 was frequently upregulated in non-small lung cancer (NSCLC) tissues compared to the adjacent nontumor tissues. CBLL1 knockdown inhibited cell invasion via increased E-cadherin protein expression, and decreased expression of MMP2 and Matrix metalloproteinase-9 (MMP9) in NSCLC cell lines. | |||
Responsed Disease | Non-small-cell lung carcinoma [ICD-11: 2C25.Y] | |||
Target Regulator | E3 ubiquitin-protein ligase Hakai (CBLL1) | WRITER | ||
In-vitro Model | A-549 | Lung adenocarcinoma | Homo sapiens | CVCL_0023 |
NCI-H1299 | Lung large cell carcinoma | Homo sapiens | CVCL_0060 | |
SK-MES-1 | Lung squamous cell carcinoma | Homo sapiens | CVCL_0630 | |
Emphysema [ICD-11: CA21]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the m6A-centered Disease Response | [1] | |||
Response Summary | METTL3-mediated formation of EV miR-93, facilitated by m6A, is implicated in the aberrant cross-talk of epithelium-macrophages, indicating that this process is involved in the smoking-related emphysema. EV miR-93 was used as a novel risk biomarker for CS-induced emphysema. MiR-93 activated the JNK pathway by targeting dual-specificity phosphatase 2 (DUSP2), which elevated the levels of Matrix metalloproteinase-9 (MMP9) and matrix metalloproteinase 12 (MMP12) and induced elastin degradation, leading to emphysema. | |||
Responsed Disease | Emphysema [ICD-11: CA21] | |||
Target Regulator | Methyltransferase-like 3 (METTL3) | WRITER | ||
Target Regulation | Down regulation | |||
Pathway Response | MAPK signaling pathway | hsa04010 | ||
Rheumatoid arthritis [ICD-11: FA20]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the m6A-centered Disease Response | [2] | |||
Response Summary | METTL3 knockdown suppressed interleukin (IL)-6, matrix metalloproteinase (MMP)-3, and Matrix metalloproteinase-9 (MMP9) levels in human RA-FLSs and rat AIA-FLSs. | |||
Responsed Disease | Rheumatoid arthritis [ICD-11: FA20] | |||
Target Regulator | Methyltransferase-like 3 (METTL3) | WRITER | ||
Target Regulation | Up regulation | |||
Cell Process | Inflammatory response | |||
In-vitro Model | FLS (Rat fibroblast synovial cell line) | |||
In-vivo Model | To establish the adjuvant-induced arthritis (AIA) model, the rats were given complete Freund's adjuvant (CFA; Chondrex, Inc.) on the left paw of 0.1 ml per 100 g of body weight. Additionally, the rats were injected with normal saline to create the negative control (NC) group. | |||
References