Molecule Information

General Information of the Molecule (ID: Mol04337)

• Name: Platelet endothelial cell adhesion molecule (PECAM1) ,Homo sapiens
• Synonyms: EndoCAM; GPIIA'; PECA1; CD_antigen=CD31
• Molecule Type: Protein
• Gene Name: PECAM1
• Gene ID: 5175
• Sequence:
  MQPRWAQGATMWLGVLLTLLLCSSLEGQENSFTINSVDMKSLPDWTVQNGKNLTLQCFAD
  VSTTSHVKPQHQMLFYKDDVLFYNISSMKSTESYFIPEVRIYDSGTYKCTVIVNNKEKT
  T AEYQVLVEGVPSPRVTLDKKEAIQGGIVRVNCSVPEEKAPIHFTIEKLELNEKMVKLK
  RE KNSRDQNFVILEFPVEEQDRVLSFRCQARIISGIHMQTSESTKSELVTVTESFSTPK
  FHI SPTGMIMEGAQLHIKCTIQVTHLAQEFPEIIIQKDKAIVAHNRHGNKAVYSVMAMV
  EHSG NYTCKVESSRISKVSSIVVNITELFSKPELESSFTHLDQGERLNLSCSIPGAPPA
  NFTIQ KEDTIVSQTQDFTKIASKSDSGTYICTAGIDKVVKKSNTVQIVVCEMLSQPRIS
  YDAQFE VIKGQTIEVRCESISGTLPISYQLLKTSKVLENSTKNSNDPAVFKDNPTEDVE
  YQCVADN CHSHAKMLSEVLRVKVIAPVDEVQISILSSKVVESGEDIVLQCAVNEGSGPI
  TYKFYREK EGKPFYQMTSNATQAFWTKQKASKEQEGEYYCTAFNRANHASSVPRSKILT
  VRVILAPWK KGLIAVVIIGVIIALLIIAAKCYFLRKAKAKQMPVEMSRPAVPLLNSNNE
  KMSDPNMEAN SHYGHNDDVRNHAMKPINDNKEPLNSDVQYTEVQVSSAESHKDLGKKDT
  ETVYSEVRKAV PDAVESRYSRTEGSLDGT
• Function: Cell adhesion molecule which is required for leukocytetransendothelial migration under most inflammatory conditions. Tyr-690 plays a critical role inTEM and is required for efficient trafficking of PECAM1 to and from thelateral border recycling compartment and is also essential forthe LBRC membrane to be targeted around migrating leukocytes. Trans-homophilic interaction may play a role inendothelial cell-cell adhesion via cell junctions .Heterophilic interaction with CD177 plays a role in transendothelialmigration of neutrophils . Homophilic ligation ofPECAM1 prevents macrophage-mediated phagocytosis of neighboring viableleukocytes by transmitting a detachment signal .Promotes macrophage-mediated phagocytosis of apoptotic leukocytes bytethering them to the phagocytic cells; PECAM1-mediated detachmentsignal appears to be disabled in apoptotic leukocytes. Modulates bradykinin receptor BDKRB2 activation. Regulates bradykinin- and hyperosmotic shock-inducedERK1/2 activation in endothelial cells . Inducessusceptibility to atherosclerosis .{ECO:0000250|UniProtKB:Q08481, ECO:0000269|PubMed:12110892,ECO:0000269|PubMed:17580308, ECO:0000269|PubMed:18672896,ECO:0000269|PubMed:19342684, ECO:0000269|PubMed:27958302}.; [Isoform Delta15]: Does not protect against apoptosis.{ECO:0000269|PubMed:18388311}.
• Uniprot ID: PECA1_HUMAN
• Ensembl ID: ENSG000002613716
• HGNC ID: HGNC:8823

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

Type(s) of Resistant Mechanism of This Molecule

  RTDM: Regulation by the Disease Microenvironment

Drug Resistance Data Categorized by Drug

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

Metformin

Drug Sensitivity Data Categorized by Their Corresponding Mechanisms

Regulation by the Disease Microenvironment (RTDM)

Disease Class: Acute myeloid leukemia [ICD-11: 2A60.0] [1]

• Sensitive Disease: Acute myeloid leukemia [ICD-11: 2A60.0]
• Sensitive Drug: Metformin
• Molecule Alteration: Expression; Down-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• In Vitro Model: KG-1 A cells; Blood; Homo sapiens (Human); CVCL_0374
• Experiment for Molecule Alteration: qPCR; qRT-PCR
• Experiment for Drug Resistance: Cell viability and proliferation assay; Cell cycle assay; Flow cytometric assay
• Mechanism Description: We found that idarubicin slightly upregulated myeloid differentiation markers, CD11b and CD14. Treatment with cytarabine, idarubicin, venetoclax, metformin, and S63845 upregulated some cell surface markers like HLA-DR expression, and metformin upregulated CD9, CD31, and CD105 cell surface marker expression. In conclusion, we believe that metformin has the potential to be used as an adjuvant in the treatment of resistant-to-first-line-chemotherapy AML cells.Also, we believe that the results of our study will stimulate further research and the potential use of changes in the expression of cell surface markers in the development of new therapeutic strategies.

References

• Ref 1: Metformin as an Enhancer for the Treatment of Chemoresistant CD34+ Acute Myeloid Leukemia Cells. Genes (Basel). 2024 May 20;15(5):648.