Molecule Information
General Information of the Molecule (ID: Mol04271)
| Name |
Glycoprotein 60 (gp60)
,Cryptosporidium parvum
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| Synonyms |
Glycoprotein 60 (gp60)
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| Molecule Type |
Protein
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Type(s) of Resistant Mechanism of This Molecule
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
| Drug Sensitivity Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Breast adenocarcinoma [ICD-11: 2C60.1] | [1] | |||
| Sensitive Disease | Breast adenocarcinoma [ICD-11: 2C60.1] | |||
| Sensitive Drug | Lapatinib | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Discovered Using In-vivo Testing Model | |||
| In Vivo Model | Athymic nude mice model | Mus musculus | ||
| Experiment for Molecule Alteration |
CD spectroscopy assay; SDS-PAGE assay | |||
| Experiment for Drug Resistance |
Cell viability assay; Fluorescence microscope assay | |||
| Mechanism Description | HER2-positive breast cancer constitutes 20 % of reported cases, characterized by excessive expression of HER2 receptors, pivotal in cell signaling and growth. Immunotherapy, the established treatment, often leads to multidrug resistance and tumor recurrence. There's a critical need for an effective strategy delaying drug resistance onset and ensuring cancer cell eradication. This study aimed to develop nanoparticles using human serum albumin (HSA) coupled with vitamin E (alpha-tocopherol succinate), loaded with a tyrosine kinase inhibitor (TKI) or aromatase inhibitor (AI). Nanoparticles were formed via desolvation, where HSA(VE) conjugates self-organized into a nanoparticle structure, incorporating TKI/AI either through chemical conjugation or direct binding to HSA. Physico-chemical analyses-such as infrared spectroscopy (IR), gel permeation chromatography (GPC), UV, IR, and CD spectroscopy confirmed HSA(VE) binding and drug incorporation into nanoparticles, evaluating their drug entrapment, release efficiency. Cell viability assays and in-vitro experiments on resistant and sensitive cell lines demonstrated effective drug encapsulation and absorption over time. Both in vitro and in vivo studies demonstrated that a combination of Lapa@HSA(VE) NPs and Let@HSA(VE) NPs in the ratio 75:25 inhibited tumor development and enhanced apoptosis significantly compared to individual NP treatment and free drug. The combination NPs therapy exhibited significant efficacy even in Lapa-resistant cell lines. | |||
References
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