Molecule Information
General Information of the Molecule (ID: Mol04116)
| Name |
Hexokinase domain containing 1 (HKDC1)
,Homo sapiens
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| Synonyms |
Hexokinase domain-containing protein 1
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| Molecule Type |
Protein
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| Gene Name |
HKDC1
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| Gene ID | |||||
| Location |
chr10:69220332-69267552[+]
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| Sequence |
MFAVHLMAFYFSKLKEDQIKKVDRFLYHMRLSDDTLLDIMRRFRAEMEKGLAKDTNPTAA
VKMLPTFVRAIPDGSENGEFLSLDLGGSKFRVLKVQVAEEGKRHVQMESQFYPTPNEIIR GNGTELFEYVADCLADFMKTKDLKHKKLPLGLTFSFPCRQTKLEEGVLLSWTKKFKARGV QDTDVVSRLTKAMRRHKDMDVDILALVNDTVGTMMTCAYDDPYCEVGVIIGTGTNACYME DMSNIDLVEGDEGRMCINTEWGAFGDDGALEDIRTEFDRELDLGSLNPGKQLFEKMISGL YLGELVRLILLKMAKAGLLFGGEKSSALHTKGKIETRHVAAMEKYKEGLANTREILVDLG LEPSEADCIAVQHVCTIVSFRSANLCAAALAAILTRLRENKKVERLRTTVGMDGTLYKIH PQYPKRLHKVVRKLVPSCDVRFLLSESGSTKGAAMVTAVASRVQAQRKQIDRVLALFQLT REQLVDVQAKMRAELEYGLKKKSHGLATVRMLPTYVCGLPDGTEKGKFLALDLGGTNFRV LLVKIRSGRRSVRMYNKIFAIPLEIMQGTGEELFDHIVQCIADFLDYMGLKGASLPLGFT FSFPCRQMSIDKGTLIGWTKGFKATDCEGEDVVDMLREAIKRRNEFDLDIVAVVNDTVGT MMTCGYEDPNCEIGLIAGTGSNMCYMEDMRNIEMVEGGEGKMCINTEWGGFGDNGCIDDI WTRYDTEVDEGSLNPGKQRYEKMTSGMYLGEIVRQILIDLTKQGLLFRGQISERLRTRGI FETKFLSQIESDRLALLQVRRILQQLGLDSTCEDSIVVKEVCGAVSRRAAQLCGAGLAAI VEKRREDQGLEHLRITVGVDGTLYKLHPHFSRILQETVKELAPRCDVTFMLSEDGSGKGA ALITAVAKRLQQAQKEN Click to Show/Hide
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| Function |
Catalyzes the phosphorylation of hexose to hexose 6- phosphate, although at very low level compared to other hexokinases (PubMed:30517626). Has low glucose phosphorylating activity compared to other hexokinases (PubMed:30517626). Involved in glucose homeostasis and hepatic lipid accumulation. Required to maintain whole-body glucose homeostasis during pregnancy; however additional evidences are required to confirm this role (By similarity). .
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| Uniprot ID | |||||
| Ensembl ID | |||||
| HGNC ID | |||||
| 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: Gastric adenocarcinoma [ICD-11: 2B72.0] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Resistant Disease | Gastric adenocarcinoma [ICD-11: 2B72.0] | |||
| Resistant Drug | Cisplatin | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Identified from the Human Clinical Data | |||
| Cell Pathway Regulation | HKDC1/G3BP7/PRKDC pathway | Regulation | N.A. | |
| In Vivo Model | HKDC1strong PRKDCstrong patients | Homo Sapiens | ||
| Experiment for Molecule Alteration |
qRT-PCR and Western blot | |||
| Experiment for Drug Resistance |
Overall survival assay (OS); Disease-free survival assay (DFS) | |||
| Mechanism Description | Taken together, in the present study, HKDC1 was showed to modulate gastric cancer metastasis and to play a pivotal role in gastric cancer chemoresistance by remodeling lipid metabolism. Our results strongly indicate that the newly identified HKDC1/G3BP1-PRKDC axis is a potential therapeutic target in GC and that specific small molecule inhibitors of PRKDC can be used to treat GC patients with high expression levels of HKDC7. | |||
| Disease Class: Gastric adenocarcinoma [ICD-11: 2B72.0] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Resistant Disease | Gastric adenocarcinoma [ICD-11: 2B72.0] | |||
| Resistant Drug | Cisplatin | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Identified from the Human Clinical Data | |||
| Cell Pathway Regulation | HKDC1/G3BP8/PRKDC pathway | Regulation | N.A. | |
| In Vivo Model | Patients with HKDC1weak/moderate PRKDCweak/moderate gastric cancer | Homo Sapiens | ||
| Experiment for Molecule Alteration |
qRT-PCR and Western blot | |||
| Experiment for Drug Resistance |
Overall survival assay (OS); Disease-free survival assay (DFS) | |||
| Mechanism Description | Taken together, in the present study, HKDC1 was showed to modulate gastric cancer metastasis and to play a pivotal role in gastric cancer chemoresistance by remodeling lipid metabolism. Our results strongly indicate that the newly identified HKDC1/G3BP1-PRKDC axis is a potential therapeutic target in GC and that specific small molecule inhibitors of PRKDC can be used to treat GC patients with high expression levels of HKDC8. | |||
| Disease Class: Gastric adenocarcinoma [ICD-11: 2B72.0] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Resistant Disease | Gastric adenocarcinoma [ICD-11: 2B72.0] | |||
| Resistant Drug | Cisplatin | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| Cell Pathway Regulation | Non-homologous end-joining | Activation | hsa03450 | |
| In Vitro Model | SGC-7901 cells | Gastric | Homo sapiens (Human) | CVCL_0520 |
| Experiment for Molecule Alteration |
qRT-PCR and Western blot | |||
| Experiment for Drug Resistance |
Cell viability assay | |||
| Mechanism Description | Taken together, in the present study, HKDC1 was showed to modulate gastric cancer metastasis and to play a pivotal role in gastric cancer chemoresistance by remodeling lipid metabolism. Our results strongly indicate that the newly identified HKDC1/G3BP1-PRKDC axis is a potential therapeutic target in GC and that specific small molecule inhibitors of PRKDC can be used to treat GC patients with high expression levels of HKDC3. | |||
| Disease Class: Gastric adenocarcinoma [ICD-11: 2B72.0] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Resistant Disease | Gastric adenocarcinoma [ICD-11: 2B72.0] | |||
| Resistant Drug | Cisplatin | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| In Vitro Model | SNU1 cells | Gastric | Homo sapiens (Human) | CVCL_0099 |
| Experiment for Molecule Alteration |
qRT-PCR and Western blot | |||
| Experiment for Drug Resistance |
Cell viability assay | |||
| Mechanism Description | Taken together, in the present study, HKDC1 was showed to modulate gastric cancer metastasis and to play a pivotal role in gastric cancer chemoresistance by remodeling lipid metabolism. Our results strongly indicate that the newly identified HKDC1/G3BP1-PRKDC axis is a potential therapeutic target in GC and that specific small molecule inhibitors of PRKDC can be used to treat GC patients with high expression levels of HKDC4. | |||
| Disease Class: Gastric adenocarcinoma [ICD-11: 2B72.0] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Resistant Disease | Gastric adenocarcinoma [ICD-11: 2B72.0] | |||
| Resistant Drug | Cisplatin | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| In Vivo Model | Peritoneal dissemination GC model in nude mice, HKDC1-overexpressing SGC-7901 cells | Mice | ||
| Experiment for Molecule Alteration |
qRT-PCR and Western blot | |||
| Experiment for Drug Resistance |
Luciferase assay | |||
| Mechanism Description | Taken together, in the present study, HKDC1 was showed to modulate gastric cancer metastasis and to play a pivotal role in gastric cancer chemoresistance by remodeling lipid metabolism. Our results strongly indicate that the newly identified HKDC1/G3BP1-PRKDC axis is a potential therapeutic target in GC and that specific small molecule inhibitors of PRKDC can be used to treat GC patients with high expression levels of HKDC5. | |||
| Disease Class: Gastric adenocarcinoma [ICD-11: 2B72.0] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Resistant Disease | Gastric adenocarcinoma [ICD-11: 2B72.0] | |||
| Resistant Drug | Cisplatin | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| In Vivo Model | Peritoneal dissemination GC model in nude mice | Mice | ||
| Experiment for Molecule Alteration |
qRT-PCR and Western blot | |||
| Experiment for Drug Resistance |
Luciferase assay | |||
| Mechanism Description | Taken together, in the present study, HKDC1 was showed to modulate gastric cancer metastasis and to play a pivotal role in gastric cancer chemoresistance by remodeling lipid metabolism. Our results strongly indicate that the newly identified HKDC1/G3BP1-PRKDC axis is a potential therapeutic target in GC and that specific small molecule inhibitors of PRKDC can be used to treat GC patients with high expression levels of HKDC6. | |||
| Drug Sensitivity Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Gastric adenocarcinoma [ICD-11: 2B72.0] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Sensitive Disease | Gastric adenocarcinoma [ICD-11: 2B72.0] | |||
| Sensitive Drug | Cisplatin | |||
| Molecule Alteration | Expression | Down-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| In Vitro Model | MKN45 cells | Liver | Homo sapiens (Human) | CVCL_0434 |
| Experiment for Molecule Alteration |
qRT-PCR and Western blot | |||
| Experiment for Drug Resistance |
Cell viability assay | |||
| Mechanism Description | Taken together, in the present study, HKDC1 was showed to modulate gastric cancer metastasis and to play a pivotal role in gastric cancer chemoresistance by remodeling lipid metabolism. Our results strongly indicate that the newly identified HKDC1/G3BP1-PRKDC axis is a potential therapeutic target in GC and that specific small molecule inhibitors of PRKDC can be used to treat GC patients with high expression levels of HKDC1. | |||
| Disease Class: Gastric adenocarcinoma [ICD-11: 2B72.0] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Sensitive Disease | Gastric adenocarcinoma [ICD-11: 2B72.0] | |||
| Sensitive Drug | Cisplatin | |||
| Molecule Alteration | Expression | Down-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| In Vitro Model | HGC27 cells | Gastric | Homo sapiens (Human) | CVCL_1279 |
| Experiment for Molecule Alteration |
qRT-PCR and Western blot | |||
| Experiment for Drug Resistance |
Cell viability assay | |||
| Mechanism Description | Taken together, in the present study, HKDC1 was showed to modulate gastric cancer metastasis and to play a pivotal role in gastric cancer chemoresistance by remodeling lipid metabolism. Our results strongly indicate that the newly identified HKDC1/G3BP1-PRKDC axis is a potential therapeutic target in GC and that specific small molecule inhibitors of PRKDC can be used to treat GC patients with high expression levels of HKDC2. | |||
References
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