Details of Drug Off-Target (DOT)

General Information of Drug Off-Target (DOT) (ID: OT57BZII)

• DOT Name: Small cell adhesion glycoprotein (SMAGP)
• Synonyms: Small transmembrane and glycosylated protein
• Gene Name: SMAGP
• Related Disease:
  Advanced cancer
  Lung cancer
  Lung carcinoma
  Metastatic malignant neoplasm
  Neoplasm
  Colorectal carcinoma
  Pancreatic adenocarcinoma
• UniProt ID: SMAGP_HUMAN
• Sequence:
  MTSLLTTPSPREELMTTPILQPTEALSPEDGASTALIAVVITVVFLTLLSVVILIFFYLY
  KNKGSYVTYEPTEGEPSAIVQMESDLAKGSEKEEYFI
• Function: May play a role in epithelial cell-cell contacts. May play a role in tumor invasiveness and metastasis formation.
• Tissue Specificity: Detected in breast, endometrium, colon and biliary tract. Detected in polarized epithelial structures characterized by cell-cell adhesion (at protein level).

Molecular Interaction Atlas (MIA) of This DOT

7 Disease(s) Related to This DOT

Disease Name	Disease ID	Evidence Level	Mode of Inheritance	REF
Advanced cancer	DISAT1Z9	Strong	Biomarker	[1]
Lung cancer	DISCM4YA	Strong	Altered Expression	[1]
Lung carcinoma	DISTR26C	Strong	Altered Expression	[1]
Metastatic malignant neoplasm	DIS86UK6	Strong	Altered Expression	[1]
Neoplasm	DISZKGEW	Strong	Altered Expression	[2]
Colorectal carcinoma	DIS5PYL0	Limited	Altered Expression	[2]
Pancreatic adenocarcinoma	DISKHX7S	Limited	Biomarker	[2]

16 Drug(s) Affected the Gene/Protein Processing of This DOT

Drug Name	Drug ID	Highest Status	Interaction	REF
Valproate	DMCFE9I	Approved	Valproate decreases the expression of Small cell adhesion glycoprotein (SMAGP).	[3]
Ciclosporin	DMAZJFX	Approved	Ciclosporin increases the expression of Small cell adhesion glycoprotein (SMAGP).	[4]
Tretinoin	DM49DUI	Approved	Tretinoin decreases the expression of Small cell adhesion glycoprotein (SMAGP).	[5]
Acetaminophen	DMUIE76	Approved	Acetaminophen decreases the expression of Small cell adhesion glycoprotein (SMAGP).	[6]
Cisplatin	DMRHGI9	Approved	Cisplatin affects the expression of Small cell adhesion glycoprotein (SMAGP).	[7]
Calcitriol	DM8ZVJ7	Approved	Calcitriol decreases the expression of Small cell adhesion glycoprotein (SMAGP).	[8]
Vorinostat	DMWMPD4	Approved	Vorinostat decreases the expression of Small cell adhesion glycoprotein (SMAGP).	[3]
Testosterone	DM7HUNW	Approved	Testosterone decreases the expression of Small cell adhesion glycoprotein (SMAGP).	[8]
Carbamazepine	DMZOLBI	Approved	Carbamazepine affects the expression of Small cell adhesion glycoprotein (SMAGP).	[9]
Decitabine	DMQL8XJ	Approved	Decitabine affects the expression of Small cell adhesion glycoprotein (SMAGP).	[7]
SNDX-275	DMH7W9X	Phase 3	SNDX-275 increases the expression of Small cell adhesion glycoprotein (SMAGP).	[10]
Genistein	DM0JETC	Phase 2/3	Genistein decreases the expression of Small cell adhesion glycoprotein (SMAGP).	[11]
(+)-JQ1	DM1CZSJ	Phase 1	(+)-JQ1 decreases the expression of Small cell adhesion glycoprotein (SMAGP).	[12]
PMID28460551-Compound-2	DM4DOUB	Patented	PMID28460551-Compound-2 decreases the expression of Small cell adhesion glycoprotein (SMAGP).	[13]
Bisphenol A	DM2ZLD7	Investigative	Bisphenol A decreases the expression of Small cell adhesion glycoprotein (SMAGP).	[14]
Trichostatin A	DM9C8NX	Investigative	Trichostatin A increases the expression of Small cell adhesion glycoprotein (SMAGP).	[15]

References

• [1] SMAGP, a new small trans-membrane glycoprotein altered in cancer.Oncogene. 2004 Apr 22;23(19):3395-403. doi: 10.1038/sj.onc.1207469.
• [2] Overexpression of the small transmembrane and glycosylated protein SMAGP supports metastasis formation of a rat pancreatic adenocarcinoma line.Int J Cancer. 2005 Dec 20;117(6):913-22. doi: 10.1002/ijc.21275.
• [3] A genomic approach to predict synergistic combinations for breast cancer treatment. Pharmacogenomics J. 2013 Feb;13(1):94-104. doi: 10.1038/tpj.2011.48. Epub 2011 Nov 15.
• [4] Integrating multiple omics to unravel mechanisms of Cyclosporin A induced hepatotoxicity in vitro. Toxicol In Vitro. 2015 Apr;29(3):489-501.
• [5] Transcriptional and Metabolic Dissection of ATRA-Induced Granulocytic Differentiation in NB4 Acute Promyelocytic Leukemia Cells. Cells. 2020 Nov 5;9(11):2423. doi: 10.3390/cells9112423.
• [6] Gene expression analysis of precision-cut human liver slices indicates stable expression of ADME-Tox related genes. Toxicol Appl Pharmacol. 2011 May 15;253(1):57-69.
• [7] Acute hypersensitivity of pluripotent testicular cancer-derived embryonal carcinoma to low-dose 5-aza deoxycytidine is associated with global DNA Damage-associated p53 activation, anti-pluripotency and DNA demethylation. PLoS One. 2012;7(12):e53003. doi: 10.1371/journal.pone.0053003. Epub 2012 Dec 27.
• [8] Effects of 1alpha,25 dihydroxyvitamin D3 and testosterone on miRNA and mRNA expression in LNCaP cells. Mol Cancer. 2011 May 18;10:58.
• [9] Gene Expression Regulation and Pathway Analysis After Valproic Acid and Carbamazepine Exposure in a Human Embryonic Stem Cell-Based Neurodevelopmental Toxicity Assay. Toxicol Sci. 2015 Aug;146(2):311-20. doi: 10.1093/toxsci/kfv094. Epub 2015 May 15.
• [10] Definition of transcriptome-based indices for quantitative characterization of chemically disturbed stem cell development: introduction of the STOP-Toxukn and STOP-Toxukk tests. Arch Toxicol. 2017 Feb;91(2):839-864.
• [11] Gene expression profiling in Ishikawa cells: a fingerprint for estrogen active compounds. Toxicol Appl Pharmacol. 2009 Apr 1;236(1):85-96.
• [12] Inhibition of BRD4 attenuates tumor cell self-renewal and suppresses stem cell signaling in MYC driven medulloblastoma. Oncotarget. 2014 May 15;5(9):2355-71.
• [13] Cell-based two-dimensional morphological assessment system to predict cancer drug-induced cardiotoxicity using human induced pluripotent stem cell-derived cardiomyocytes. Toxicol Appl Pharmacol. 2019 Nov 15;383:114761. doi: 10.1016/j.taap.2019.114761. Epub 2019 Sep 15.
• [14] Bisphenol A induces DSB-ATM-p53 signaling leading to cell cycle arrest, senescence, autophagy, stress response, and estrogen release in human fetal lung fibroblasts. Arch Toxicol. 2018 Apr;92(4):1453-1469.
• [15] From transient transcriptome responses to disturbed neurodevelopment: role of histone acetylation and methylation as epigenetic switch between reversible and irreversible drug effects. Arch Toxicol. 2014 Jul;88(7):1451-68.