General Information of the Molecule (ID: Mol04059)
Name
Choline-phosphate cytidylyltransferase A (CCTalpha) ,Homo sapiens
Synonyms
CCT-alpha; CTP:phosphocholine cytidylyltransferase A; Phosphorylcholine transferase A
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Molecule Type
Protein
Gene Name
PCYT1A
Gene ID
5130
Location
chr3:196214222-196287957[-]
Sequence
MDAQCSAKVNARKRRKEAPGPNGATEEDGVPSKVQRCAVGLRQPAPFSDEIEVDFSKPYV
RVTMEEASRGTPCERPVRVYADGIFDLFHSGHARALMQAKNLFPNTYLIVGVCSDELTHN
FKGFTVMNENERYDAVQHCRYVDEVVRNAPWTLTPEFLAEHRIDFVAHDDIPYSSAGSDD
VYKHIKEAGMFAPTQRTEGISTSDIITRIVRDYDVYARRNLQRGYTAKELNVSFINEKKY
HLQERVDKVKKKVKDVEEKSKEFVQKVEEKSIDLIQKWEEKSREFIGSFLEMFGPEGALK
HMLKEGKGRMLQAISPKQSPSSSPTRERSPSPSFRWPFSGKTSPPCSPANLSRHKAAAYD
ISEDEED
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Function
Catalyzes the key rate-limiting step in the CDP-choline pathway for phosphatidylcholine biosynthesis. .
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Uniprot ID
PCY1A_HUMAN
Ensembl ID
ENSG00000161217
HGNC ID
HGNC:8754
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Kingdom: Metazoa
Phylum: Chordata
Class: Mammalia
Order: Primates
Family: Hominidae
Genus: Homo
Species: Homo sapiens
Type(s) of Resistant Mechanism of This Molecule
  MRAP: Metabolic Reprogramming via Altered Pathways
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
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Hydroxyflutamide
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
  Metabolic Reprogramming via Altered Pathways (MRAP) Click to Show/Hide
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
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
Ref 1 Resistance to 2-Hydroxy-Flutamide in Prostate Cancer Cells Is Associated with the Downregulation of Phosphatidylcholine Biosynthesis and Epigenetic Modifications. Int J Mol Sci. 2023 Oct 26;24(21):15626.

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