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PMID:30873824

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Citation

Wang, J, Yang, L, Liang, F, Chen, Y and Yang, G (2019) Integrin alpha x stimulates cancer angiogenesis through PI3K/Akt signaling-mediated VEGFR2/VEGF-A overexpression in blood vessel endothelial cells. J. Cell. Biochem. 120:1807-1818

Abstract

Integrin alpha x (ITGAX), a member of the integrin family, usually serves as a receptor of the extracellular matrix. Recently, accumulating evidence suggests that ITGAX may be involved in angiogenesis in dendritic cells. Herein, we report a direct role of ITGAX in angiogenesis during tumor development. Overexpression of ITGAX in human umbilical vein endothelial cells (HUVECs) enhanced their proliferation, migration, and tube formation and promoted xenograft ovarian tumor angiogenesis and growth. Further study showed that overexpression of ITGAX activated the PI3k/Akt pathway, leading to the enhanced expression of c-Myc, vascular endothelial growth factor-A (VEGF-A), and VEGF receptor 2 (VEGFR2), whereas, the treatment of cells with PI3K inhibitor diminished these effects. Besides, c-Myc was observed to bind to the VEGF-A promoter. By Co-Immunoprecipitation (Co-IP) assay, we manifested the interaction between ITGAX and VEGFR2 or the phosphorylated VEGFR2. Immunostaining of human ovarian cancer specimens suggested that endothelial cells of micro-blood vessels displayed strong expression of VEGF-A, c-Myc, VEGFR2, and the PI3K signaling molecules. Also, overexpression of ITGAX in HUVECs could stimulate the spheroid formation of ovarian cancer cells. Our study uncovered that ITGAX stimulates angiogenesis through the PI3K/Akt signaling-mediated VEGFR2/VEGF-A overexpression during cancer development.

Links

PubMed Online version:10.1002/jcb.27480

Keywords


Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

HUMAN:MYC

enables

GO:0001046: core promoter sequence-specific DNA binding

ECO:0000314: direct assay evidence used in manual assertion

F

  • has_input:(UniProtKB:P15692)
  • occurs_in:(CL:0002618)

Seeded From UniProt

complete

HUMAN:ITAX

involved_in

GO:0010628: positive regulation of gene expression

ECO:0000315: mutant phenotype evidence used in manual assertion

P

  • has_input:(UniProtKB:P15692)
  • regulates_o_occurs_in:(CL:0002618)|has_input(UniProtKB:P27986)
  • regulates_o_occurs_in:(CL:0002618)|has_input(UniProtKB:P31749)
  • regulates_o_occurs_in:(CL:0002618)|has_input(UniProtKB:P01106)
  • regulates_o_occurs_in:(CL:0002618)|has_input(UniProtKB:P35968)
  • regulates_o_occurs_in:(CL:0002618)|has_input(UniProtKB:P61073)
  • regulates_o_occurs_in:(CL:0002618)

Seeded From UniProt

complete

HUMAN:ITAX

involved_in

GO:0030335: positive regulation of cell migration

ECO:0000315: mutant phenotype evidence used in manual assertion

P

  • regulates_o_occurs_in:(CL:0002618)

Seeded From UniProt

complete

HUMAN:ITAX

enables

GO:0030971: receptor tyrosine kinase binding

ECO:0000353: physical interaction evidence used in manual assertion

UniProtKB:P35968

F

Seeded From UniProt

complete

HUMAN:ITAX

involved_in

GO:0008284: positive regulation of cell population proliferation

ECO:0000315: mutant phenotype evidence used in manual assertion

P

  • regulates_o_occurs_in:(CL:0002618)

Seeded From UniProt

complete

HUMAN:ITAX

involved_in

GO:0045766: positive regulation of angiogenesis

ECO:0000315: mutant phenotype evidence used in manual assertion

P

  • regulates_o_occurs_in:(UBERON:0005335)

Seeded From UniProt

complete

HUMAN:ITAX

involved_in

GO:1905956: positive regulation of endothelial tube morphogenesis

ECO:0000315: mutant phenotype evidence used in manual assertion

P

  • regulates_o_occurs_in:(CL:0002618)

Seeded From UniProt

complete

HUMAN:MYC

enables

GO:0001047: core promoter binding

ECO:0000353: physical interaction evidence used in manual assertion

UniProtKB:P15692

F

Seeded From UniProt

complete

HUMAN:VGFR2

enables

GO:0005178: integrin binding

ECO:0000353: physical interaction evidence used in manual assertion

UniProtKB:P20702

F

Seeded From UniProt

complete

Notes

See also

References

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