Disease Information
General Information of the Disease (ID: DIS00534)
| Name |
Breast cancer
|
|---|---|
| ICD |
ICD-11: 2C60
|
| Resistance Map |
Type(s) of Resistant Mechanism of This Disease
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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| Key Molecule: Sodium/glucose cotransporter 1 (SGLT1) | [1] | |||
| Metabolic Type | Glucose metabolism | |||
| Resistant Disease | Estrogen receptor (ER)-positive breast cancer [ICD-11: 2C60.6] | |||
| Resistant Drug | Tamoxifen | |||
| Molecule Alteration | Expression | Up-regulation |
||
| Experimental Note | Identified from the Human Clinical Data | |||
| In Vivo Model | Estrogen receptor (ER)-positive breast cancer patient | Homo Sapiens | ||
| Experiment for Molecule Alteration |
Western blot analysis | |||
| Experiment for Drug Resistance |
Cell prognosis assay | |||
| Mechanism Description | Here, we characterized sodium/glucose cotransporter 1 (SGLT1) overexpression drives the highly glycolytic phenotype of tamoxifen-resistant breast cancer cells where enhanced lactic acid secretion promotes M2-like TAM polarization via the hypoxia-inducible factor-1alpha/signal transducer and activator of transcription-4 pathway | |||
| Key Molecule: Sodium/glucose cotransporter 1 (SGLT1) | [1] | |||
| Metabolic Type | Glucose metabolism | |||
| Resistant Disease | Estrogen receptor (ER)-positive breast cancer [ICD-11: 2C60.6] | |||
| Resistant Drug | Tamoxifen | |||
| Molecule Alteration | Expression | Up-regulation |
||
| Experimental Note | Revealed Based on the Cell Line Data | |||
| In Vitro Model | MCF7 cells | Breast | Homo sapiens (Human) | CVCL_0031 |
| Experiment for Molecule Alteration |
Western blot analysis | |||
| Experiment for Drug Resistance |
CCK8 assay | |||
| Mechanism Description | Here, we characterized sodium/glucose cotransporter 1 (SGLT1) overexpression drives the highly glycolytic phenotype of tamoxifen-resistant breast cancer cells where enhanced lactic acid secretion promotes M2-like TAM polarization via the hypoxia-inducible factor-1alpha/signal transducer and activator of transcription-3 pathway | |||
| Key Molecule: Sodium/glucose cotransporter 1 (SGLT1) | [1] | |||
| Metabolic Type | Glucose metabolism | |||
| Resistant Disease | Estrogen receptor (ER)-positive breast cancer [ICD-11: 2C60.6] | |||
| Resistant Drug | Tamoxifen | |||
| Molecule Alteration | Expression | Up-regulation |
||
| Experimental Note | Revealed Based on the Cell Line Data | |||
| In Vitro Model | T-47D cells | N.A. | Homo sapiens (Human) | CVCL_0553 |
| Experiment for Molecule Alteration |
Western blot analysis | |||
| Experiment for Drug Resistance |
CCK8 assay | |||
| Mechanism Description | Here, we characterized sodium/glucose cotransporter 1 (SGLT1) overexpression drives the highly glycolytic phenotype of tamoxifen-resistant breast cancer cells where enhanced lactic acid secretion promotes M2-like TAM polarization via the hypoxia-inducible factor-1alpha/signal transducer and activator of transcription-4 pathway | |||
References
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