Molecule Information

General Information of the Molecule (ID: Mol00193)

• Name: EGFR-coamplified and overexpressed protein (ECOP) ,Homo sapiens
• Synonyms: EGFR-coamplified and overexpressed protein; ECop; Glioblastoma-amplified secreted protein; Putative NF-kappa-B-activating protein 055N; ECOP; GASP
• Molecule Type: Protein
• Gene Name: VOPP1
• Gene ID: 81552
• Location: chr7:55436056-55572988[-]
• Sequence:
  MRRQPAKVAALLLGLLLECTEAKKHCWYFEGLYPTYYICRSYEDCCGSRCCVRALSIQRL
  WYFWFLLMMGVLFCCGAGFFIRRRMYPPPLIEEPAFNVSYTRQPPNPGPGAQQPGPPYYT
  DPGGPGMNPVGNSMAMAFQVPPNSPQGSVACPPPPAYCNTPPPPYEQVVKAK
• Function: Increases the transcriptional activity of NFKB1 by facilitating its nuclear translocation, DNA-binding and associated apoptotic response, when overexpressed.
• Uniprot ID: VOPP1_HUMAN
• Ensembl ID: ENSG00000154978
• HGNC ID: HGNC:34518

Kingdom: Metazoa
Phylum: Chordata
Class: Mammalia
Order: Primates
Family: Hominidae
Genus: Homo
Species: Homo sapiens

Type(s) of Resistant Mechanism of This Molecule

  UAPP: Unusual Activation of Pro-survival Pathway

Drug Resistance Data Categorized by Drug

Approved Drug(s) 1 drug(s) in total

Fluorouracil

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Unusual Activation of Pro-survival Pathway (UAPP)

Disease Class: Colorectal cancer [ICD-11: 2B91.1] [1]

• Resistant Disease: Colorectal cancer [ICD-11: 2B91.1]
• Resistant Drug: Fluorouracil
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• Cell Pathway Regulation: Cell metastasis; Activation; hsa05205
• Cell Pathway Regulation: NF-kB signaling pathway; Activation; hsa04218
• In Vitro Model: HT29 Cells; Colon; Homo sapiens (Human); CVCL_A8EZ
• In Vitro Model: SW480 cells; Colon; Homo sapiens (Human); CVCL_0546
• Experiment for Molecule Alteration: Western blot analysis; luciferase reporter assay;ChIP
• Experiment for Drug Resistance: CCK8 assay
• Mechanism Description: VOPP1 overexpression partially reversed the miR-218-induced enhanced susceptibility to 5FU in the HT29 5FU-R subline and HOTAIR knockdown partially reversed 5FU resistance through promoting miR-218 and inactivating NF-kB signaling.

Disease Class: Colorectal cancer [ICD-11: 2B91.1] [1]

• Resistant Disease: Colorectal cancer [ICD-11: 2B91.1]
• Resistant Drug: Fluorouracil
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• Cell Pathway Regulation: NF-kB signaling pathway; Activation; hsa04218
• In Vitro Model: HT29 Cells; Colon; Homo sapiens (Human); CVCL_A8EZ
• In Vitro Model: SW480 cells; Colon; Homo sapiens (Human); CVCL_0546
• In Vitro Model: FHC cells; Colon; Homo sapiens (Human); CVCL_3688
• Experiment for Molecule Alteration: qPCR
• Experiment for Drug Resistance: CCK8 assay; Colony formation assays
• Mechanism Description: LncRNA HOTAIR contributes to 5fu resistance through suppressing miR-218 and the activation of VOPP1 expression and activating NF-kB/TS signaling in colorectal cancer.

References

• Ref 1: lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-kB/TS Signaling in Colorectal Cancer. Mol Ther Nucleic Acids. 2017 Sep 15;8:356-369. doi: 10.1016/j.omtn.2017.07.007. Epub 2017 Jul 8.