General Information of the Molecule (ID: Mol00678)
Name
Tumor necrosis factor ligand superfamily member 10 (TNFSF10) ,Homo sapiens
Molecule Type
Protein
Gene Name
TNFSF10
Gene ID
8743
Location
chr3:172505508-172523475[-]
Sequence
MAMMEVQGGPSLGQTCVLIVIFTVLLQSLCVAVTYVYFTNELKQMQDKYSKSGIACFLKE
DDSYWDPNDEESMNSPCWQVKWQLRQLVRKMILRTSEETISTVQEKQQNISPLVRERGPQ
RVAAHITGTRGRSNTLSSPNSKNEKALGRKINSWESSRSGHSFLSNLHLRNGELVIHEKG
FYYIYSQTYFRFQEEIKENTKNDKQMVQYIYKYTSYPDPILLMKSARNSCWSKDAEYGLY
SIYQGGIFELKENDRIFVSVTNEHLIDMDHEASFFGAFLVG
    Click to Show/Hide
Function
Cytokine that binds to TNFRSF10A/TRAILR1, TNFRSF10B/TRAILR2, TNFRSF10C/TRAILR3, TNFRSF10D/TRAILR4 and possibly also to TNFRSF11B/OPG. Induces apoptosis. Its activity may be modulated by binding to the decoy receptors TNFRSF10C/TRAILR3, TNFRSF10D/TRAILR4 and TNFRSF11B/OPG that cannot induce apoptosis.
    Click to Show/Hide
Uniprot ID
TNF10_HUMAN
Ensembl ID
ENSG00000121858
HGNC ID
HGNC:11925
        Click to Show/Hide the Complete Species Lineage
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
Click to Show/Hide the Full List of Drugs
Docetaxel
Click to Show/Hide
Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Unusual Activation of Pro-survival Pathway (UAPP) Click to Show/Hide
Disease Class: Prostate cancer [1]
Resistant Disease Prostate cancer [ICD-11: 2C82.0]
Resistant Drug Docetaxel
Molecule Alteration Expression
Down-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell apoptosis Inhibition hsa04210
Cell proliferation Activation hsa05200
In Vitro Model LNCaP cells Prostate Homo sapiens (Human) CVCL_0395
VCaP cells Prostate Homo sapiens (Human) CVCL_2235
LTAD cells Prostate Homo sapiens (Human) N.A.
Experiment for
Molecule Alteration
Western blot analysis; Immunohistochemistry assay
Experiment for
Drug Resistance
TUNEL assay; MTS assay
Mechanism Description Androgen-induced Long Noncoding RNA (LncRNA) SOCS2-AS1 Promotes Cell Growth and Inhibits Apoptosis in Prostate Cancer Cells.suppressor of cytokine signaling 2-antisense transcript 1 (SOCS2-AS1), the expression of which was higher in castration-resistant prostate cancer model cells.SOCS2-AS1 promoted castration-resistant and androgen-dependent cell growth. We found that SOCS2-AS1 knockdown up-regulated genes related to the apoptosis pathway, including tumor necrosis factor superfamily 10 (TNFSF10), and sensitized prostate cancer cells to docetaxel treatment. Moreover, we also demonstrated that SOCS2-AS1 promotes androgen signaling by modulating the epigenetic control for AR target genes including TNFSF10 These findings suggest that SOCS2-AS1 plays an important role in the development of castration-resistant prostate cancer by repressing apoptosis.
Disease- and Tissue-specific Abundances of This Molecule
ICD Disease Classification 02
Click to Show/Hide the Resistance Disease of This Class
Prostate cancer [ICD-11: 2C82]
Click to Show/Hide
Differential expression of molecule in resistant diseases
The Studied Tissue Prostate
The Specified Disease Prostate cancer
The Expression Level of Disease Section Compare with the Healthy Individual Tissue p-value: 9.66E-01; Fold-change: 1.85E-01; Z-score: 3.72E-01
Molecule expression in the diseased tissue of patients
Molecule expression in the normal tissue of healthy individuals
Disease-specific Molecule Abundances Click to View the Clearer Original Diagram
Tissue-specific Molecule Abundances in Healthy Individuals
Click to Show/Hide the Molecule Abundances
References
Ref 1 Androgen-induced Long Noncoding RNA (lncRNA) SOCS2-AS1 Promotes Cell Growth and Inhibits Apoptosis in Prostate Cancer Cells. J Biol Chem. 2016 Aug 19;291(34):17861-80. doi: 10.1074/jbc.M116.718536. Epub 2016 Jun 24.

If you find any error in data or bug in web service, please kindly report it to Dr. Sun and Dr. Zhang.