Bigh3 silencing increases retinoblastoma tumor growth in the murine SV40-TAg-Rb model

Oncotarget. 2017 Feb 28;8(9):15490-15506. doi: 10.18632/oncotarget.14659.

Abstract

BIGH3, a secreted protein of the extracellular matrix interacts with collagen and integrins on the cell surface. BIGH3 can have opposing functions in cancer, acting either as tumor suppressor or promoter by enhancing tumor progression and angiogenesis. In the eye, BIGH3 is expressed in the cornea and the retinal pigment epithelium and could impact on the development of retinoblastoma, the most common paediatric intraocular neoplasm. Retinoblastoma initiation requires the inactivation of both alleles of the RB1 tumor suppressor gene in the developing retina and tumor progression involves additional genomic changes. To determine whether BIGH3 affects retinoblastoma development, we generated a retinoblastoma mouse model with disruption of the Bigh3 genomic locus. Bigh3 silencing in these mice resulted in enhanced tumor development in the retina. A decrease in apoptosis is involved in the initial events of tumorigenesis, followed by an increased activity of the pro-survival ERK pathway as well as an upregulation of cyclin-dependent kinases (CDKs). Taken together, these data suggest that BIGH3 acts as a tumor suppressor in the retina.

Keywords: BIGH3; SV40-TAg-Rb mice; cancer; retinoblastoma.

MeSH terms

  • Animals
  • Antigens, Polyomavirus Transforming / genetics*
  • Apoptosis / genetics
  • Blotting, Western
  • Cyclin-Dependent Kinases / genetics
  • Cyclin-Dependent Kinases / metabolism
  • Disease Models, Animal*
  • Extracellular Matrix Proteins / genetics*
  • Extracellular Matrix Proteins / metabolism
  • Humans
  • MAP Kinase Signaling System / genetics
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Transgenic
  • Microscopy, Fluorescence
  • Retinal Neoplasms / genetics*
  • Retinal Neoplasms / metabolism
  • Retinal Neoplasms / pathology
  • Retinal Pigment Epithelium / metabolism
  • Retinal Pigment Epithelium / pathology
  • Retinoblastoma / genetics*
  • Retinoblastoma / metabolism
  • Retinoblastoma / pathology
  • Retinoblastoma Protein / genetics
  • Retinoblastoma Protein / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transforming Growth Factor beta / genetics*
  • Transforming Growth Factor beta / metabolism
  • Tumor Burden / genetics
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism

Substances

  • Antigens, Polyomavirus Transforming
  • Extracellular Matrix Proteins
  • Retinoblastoma Protein
  • Transforming Growth Factor beta
  • Tumor Suppressor Proteins
  • betaIG-H3 protein
  • Cyclin-Dependent Kinases