Molecule Information
General Information of the Molecule (ID: Mol04012)
| Name |
Adrenomedullin (ADM)
,Homo sapiens
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| Molecule Type |
Protein
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| Gene Name |
ADM5
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| Gene ID | |||||
| Location |
chr19:49689594-49690575[+]
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| Sequence |
MTIHILILLLLLAFSAQGDLDTAARRGQHQVPQHRGHVCYLGVCRTHRLAEIIYWIRCLH
QGALGEGQPRAPGPLQLWAPPVARGGSPARFPGFRPAARGLAQCPARWVTSGTARPLLGF SLPICMLELLLHISSPLTPAPETVFPSPSPGCD Click to Show/Hide
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| Function |
Probable non-functional remnant of adrenomedullin-5. .
Click to Show/Hide
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| Uniprot ID | |||||
| Ensembl ID | |||||
| HGNC ID | |||||
| Click to Show/Hide the Complete Species Lineage | |||||
Type(s) of Resistant Mechanism of This Molecule
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Ovarian cancer [ICD-11: 2C73.0] | [1] | |||
| Metabolic Type | Glucose metabolism | |||
| Resistant Disease | Ovarian cancer [ICD-11: 2C73.0] | |||
| Resistant Drug | Cisplatin | |||
| Molecule Alteration | Expression | Up-regulation |
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| Differential expression of the molecule in resistant disease | ||||
| Classification of Disease | Ovarian cancer [ICD-11: 2C73] | |||
| The Specified Disease | Ovarian cancer | |||
| The Studied Tissue | Blood | |||
| The Expression Level of Disease Section Compare with the Healthy Individual Tissue | p-value: 2.98E-25 Fold-change: 3.57E-01 Z-score: 1.20E+01 |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| In Vitro Model | A2780CIS cells | Ovary | Homo sapiens (Human) | CVCL_1942 |
| Experiment for Molecule Alteration |
RNA seq | |||
| Experiment for Drug Resistance |
CCK8 assay | |||
| Mechanism Description | The present study demonstrated that ADM can induce cisplatin chemoresistance in human ovarian epithelial carcinoma cells through reprogramming of glucose metabolism via upregulation of PKM2 and subsequently contribute to cancer prevention and therapy. This conclusion is supported by the following observations: (1)ADMexpression was upregulated in cisplatin-resistant EOC cells; (2) ADM attenuated cisplatin-inhibited cell survival and cisplatin-induced apoptosis in sensitive EOC cells; (3) knockdown of ADM enhanced cisplatin chemosensitivity of cisplatin-resistant EOC cells; (4) ADM enhanced glycolysis in cisplatin-sensitive EOC cells; (5) knockdown of ADM significantly inhibited glycolysis in cisplatin-resistant EOC cells; and (6) ADM significantly upregulated PKM2 protein level, the key enzyme during glycolysis. | |||
| Disease Class: Ovarian cancer [ICD-11: 2C73.0] | [1] | |||
| Metabolic Type | Glucose metabolism | |||
| Resistant Disease | Ovarian cancer [ICD-11: 2C73.0] | |||
| Resistant Drug | Cisplatin | |||
| Molecule Alteration | Expression | Up-regulation |
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| Differential expression of the molecule in resistant disease | ||||
| Classification of Disease | Ovarian cancer [ICD-11: 2C73] | |||
| The Specified Disease | Ovarian cancer | |||
| The Studied Tissue | Blood | |||
| The Expression Level of Disease Section Compare with the Healthy Individual Tissue | p-value: 2.98E-25 Fold-change: 3.57E-01 Z-score: 1.20E+01 |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| In Vitro Model | A2780 EOC cells | Ovary | Homo sapiens (Human) | CVCL_0134 |
| Experiment for Molecule Alteration |
RNA seq | |||
| Experiment for Drug Resistance |
CCK8 assay | |||
| Mechanism Description | The present study demonstrated that ADM can induce cisplatin chemoresistance in human ovarian epithelial carcinoma cells through reprogramming of glucose metabolism via upregulation of PKM2 and subsequently contribute to cancer prevention and therapy. This conclusion is supported by the following observations: (1) ADM expression was upregulated in cisplatin-resistant EOC cells; (2) ADM attenuated cisplatin-inhibited cell survival and cisplatin-induced apoptosis in sensitive EOC cells; (3) knockdown of ADM enhanced cisplatin chemosensitivity of cisplatin-resistant EOC cells; (4) ADM enhanced glycolysis in cisplatin-sensitive EOC cells; (5) knockdown of ADM significantly inhibited glycolysis in cisplatin-resistant EOC cells; and (6) ADM significantly upregulated PKM2 protein level, the key enzyme during glycolysis. | |||
References
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