The role of KDR in the interactions between human gastric carcinoma cell and vascular endothelial cell

Juan Ren1, Lei Dong, Cang-Bao Xu

  • 1Department of Oncological Radiotherapy,First Hospital,Xi'an Jiaotong University Xi'an 710061,Shaanxi Province, China. renjuan88@163.net

Abstract

Insights

KDR plays a key role in human gastric carcinoma cell (HGCC) and human vascular endothelial cell (HVEC) interactions. Inhibiting KDR significantly affects HGCC and HVEC proliferation, revealing complex cross-talk between these cell types.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Human gastric carcinoma cells (HGCC) and human vascular endothelial cells (HVEC) interact in complex ways.
  • The role of KDR (Kinase insert domain receptor) in these interactions is not fully understood.

Purpose of the Study:

  • To investigate the interactions between HGCC and HVEC.
  • To elucidate the specific role of KDR in regulating the proliferation and interaction of these cells.

Main Methods:

  • Antisense oligodeoxynucleotide (ASODN) specific to the KDR gene was used to inhibit KDR expression in HGCC and HVEC.
  • Cell proliferation was assessed using the MTT assay.
  • Conditioned media (CM) from HGCC and HVEC were used to study their effects on each other.
  • KDR gene expression (mRNA and protein) and human vascular endothelial growth factor (hVEGF) levels were analyzed using in situ hybridization, immunohistochemical staining, and ABC-ELISA.

Main Results:

  • KDR ASODN significantly inhibited the proliferation of both HGCC (55.35%) and HVEC (54.83%).
  • HGCC and HVEC secreted hVEGF (92.06 ng/L and 77.70 ng/L, respectively).
  • HGCC-CM stimulated HVEC growth and KDR expression, while HVEC-CM inhibited HGCC growth and KDR expression.

Conclusions:

  • KDR is a critical regulator of HGCC and HVEC proliferation.
  • Complex interactions exist between HGCC and HVEC, with HGCC stimulating HVEC growth and HVEC inhibiting HGCC growth.
  • KDR is involved in mediating these reciprocal interactions between gastric carcinoma cells and vascular endothelial cells.

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