Molecule Information
General Information of the Molecule (ID: Mol04183)
| Name |
microRNA-494 (miR-494)
,Homo sapiens
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| Synonyms |
microRNA 494
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| Molecule Type |
Mature miRNA
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| Ensembl ID | |||||
| HGNC ID | |||||
| Mature Accession | |||||
| 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: Hepatocellular carcinoma [ICD-11: 2C12.02] | [1] | |||
| Metabolic Type | Glucose metabolism | |||
| Resistant Disease | Hepatocellular carcinoma [ICD-11: 2C12.02] | |||
| Resistant Drug | Sorafenib | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Identified from the Human Clinical Data | |||
| Cell Pathway Regulation | HIF-1 signaling pathway | Activation | hsa04066 | |
| In Vivo Model | HCC patient | Homo Sapiens | ||
| Experiment for Molecule Alteration |
Real time PCR | |||
| Experiment for Drug Resistance |
Overall survival assay (OS) | |||
| Mechanism Description | MiR-494 induced the metabolic shift of HCC cells toward a glycolytic phenotype through G6pc targeting and HIF-1A pathway activation. MiR-494/G6pc axis played an active role in metabolic plasticity of cancer cells, leading to glycogen and lipid droplets accumulation that favored cell survival under harsh environmental conditions. | |||
| Disease Class: Hepatocellular carcinoma [ICD-11: 2C12.02] | [1] | |||
| Metabolic Type | Glucose metabolism | |||
| Resistant Disease | Hepatocellular carcinoma [ICD-11: 2C12.02] | |||
| Resistant Drug | Sorafenib | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| Cell Pathway Regulation | HIF-1 signaling pathway | Activation | hsa04066 | |
| In Vitro Model | Huh7 cells | Kidney | Homo sapiens (Human) | CVCL_U442 |
| Experiment for Molecule Alteration |
Real time PCR | |||
| Experiment for Drug Resistance |
Cell viability assay | |||
| Mechanism Description | MiR-494 induced the metabolic shift of HCC cells toward a glycolytic phenotype through G6pc targeting and HIF-1A pathway activation. MiR-494/G6pc axis played an active role in metabolic plasticity of cancer cells, leading to glycogen and lipid droplets accumulation that favored cell survival under harsh environmental conditions. | |||
| Disease Class: Hepatocellular carcinoma [ICD-11: 2C12.02] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Resistant Disease | Hepatocellular carcinoma [ICD-11: 2C12.02] | |||
| Resistant Drug | Sorafenib | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| Experiment for Molecule Alteration |
qRT-PCR; Western blot analysis | |||
| Experiment for Drug Resistance |
Spheroids formation assay | |||
| Mechanism Description | Here, we confirmed the synergic effect of antimiR-494/sorafenib treatment and demonstrated for the first time that, together with AKT pathway repression, G6pc targeting mediates miR-494-induced sorafenib resistance in HCC cells. In line, the oncomiR-21 triggered sorafenib resistance in HCC cells by PTEN direct targeting or by regulating the nuclear localization of the long non-coding RNA SNHG1 [63]. | |||
| Disease Class: Hepatocellular carcinoma [ICD-11: 2C12.02] | [1] | |||
| Metabolic Type | Glucose metabolism | |||
| Resistant Disease | Hepatocellular carcinoma [ICD-11: 2C12.02] | |||
| Resistant Drug | Sorafenib | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| Cell Pathway Regulation | HIF-1 signaling pathway | Activation | hsa04066 | |
| In Vivo Model | Diethylnitrosamine (DEN)-induced HCC rats; Diethylnitrosamine (DEN)-induced xenograft mice | Mice; Rats | ||
| Experiment for Molecule Alteration |
Real time PCR | |||
| Experiment for Drug Resistance |
Tumor volume assay | |||
| Mechanism Description | MiR-494 induced the metabolic shift of HCC cells toward a glycolytic phenotype through G6pc targeting and HIF-1A pathway activation. MiR-494/G6pc axis played an active role in metabolic plasticity of cancer cells, leading to glycogen and lipid droplets accumulation that favored cell survival under harsh environmental conditions. | |||
References
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