Molecule Information
General Information of the Molecule (ID: Mol04059)
| Name |
Choline-phosphate cytidylyltransferase A (CCTalpha)
,Homo sapiens
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| Synonyms |
CCT-alpha; CTP:phosphocholine cytidylyltransferase A; Phosphorylcholine transferase A
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| Molecule Type |
Protein
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| Gene Name |
PCYT1A
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| Gene ID | |||||
| Location |
chr3:196214222-196287957[-]
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| Sequence |
MDAQCSAKVNARKRRKEAPGPNGATEEDGVPSKVQRCAVGLRQPAPFSDEIEVDFSKPYV
RVTMEEASRGTPCERPVRVYADGIFDLFHSGHARALMQAKNLFPNTYLIVGVCSDELTHN FKGFTVMNENERYDAVQHCRYVDEVVRNAPWTLTPEFLAEHRIDFVAHDDIPYSSAGSDD VYKHIKEAGMFAPTQRTEGISTSDIITRIVRDYDVYARRNLQRGYTAKELNVSFINEKKY HLQERVDKVKKKVKDVEEKSKEFVQKVEEKSIDLIQKWEEKSREFIGSFLEMFGPEGALK HMLKEGKGRMLQAISPKQSPSSSPTRERSPSPSFRWPFSGKTSPPCSPANLSRHKAAAYD ISEDEED Click to Show/Hide
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| Function |
Catalyzes the key rate-limiting step in the CDP-choline pathway for phosphatidylcholine biosynthesis. .
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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 Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Prostate cancer [ICD-11: 2C82.0] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Resistant Disease | Prostate cancer [ICD-11: 2C82.0] | |||
| Resistant Drug | Hydroxyflutamide | |||
| Molecule Alteration | Expression | Down-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| Cell Pathway Regulation | Biosynthesis of secondary metabolites | Activation | hsa01110 | |
| In Vitro Model | LNCaP cells | Prostate | Homo sapiens (Human) | CVCL_0395 |
| PC-3 cells | Bone | Homo sapiens (Human) | CVCL_0035 | |
| Experiment for Molecule Alteration |
qRT-PCR; Western blot analysis | |||
| Experiment for Drug Resistance |
Cell viability assay | |||
| Mechanism Description | Our study shows that the long-term treatment of androgen-sensitive prostate cancer cells with the antiandrogen 2-hydroxy-flutamide leads to the development of a quiescent state with stem cell-like characteristics, enabling survival in a low metabolic state and conferring drug resistance. In this context, there is a reduction in the de novo biosynthesis of phosphatidylcholine and the activation of epigenetic reprogramming. | |||
References
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