Expression of human granulocyte colony stimulating factor (hG-CSF) in colon adenocarcinoma cell line (Caco-2)

Snehasis Jana,Hitesh Patel

doi:10.1007/s10529-012-0977-5

Abstract

Growth and progression of many cancer cells are mediated by alterations in the microenvironment often caused by an aberrant expression of growth factors and receptors. There is no report on expression of growth factor granulocyte colony-stimulating factor (G-CSF) in the experimental model, colon adenocarcinoma cell line (Caco2), that is commonly used in drug permeability assays. We hypothesize that in vitro, the Caco2 model is associated with a constitutive neo-expression of the hematopoietic G-CSF thereby causing an autocrine stimulation of Caco2 growth and proliferation in vitro. To test our hypothesis, we analyzed mRNA and protein expression of G-CSF in Caco2 cells using reverse transcriptase-PCR and SDS-PAGE. G-CSF mRNA and protein were detected in Caco2 cells. Expression of G-CSF protein was similar at different passages of this cell line. The expression of G-CSF has a significant role in the autocrine regulation of Caco2 cell growth and proliferation.

Highlights

Cancer is often the result of an unregulated expression of growth factors (Mueller et al 1999) that stimulate tumor cell proliferation and/or stromal activation and angiogenesis through autocrine or paracrine loops with the appropriate receptor-bearing cells (Mueller et al 2001)
There is no report on expression of growth factor granulocyte colony-stimulating factor (G-CSF) in the experimental model, colon adenocarcinoma cell line (Caco2), that is commonly used in drug permeability assays
Beside its function as growth and differentiation factors of the hematopoietic system, G-CSF is expressed by fibroblasts (Moore 1991), endothelial cells (Kikuchi et al 1996), and keratinocytes (Mann et al 2001)

Summary

Introduction

Cancer is often the result of an unregulated expression of growth factors (Mueller et al 1999) that stimulate tumor cell proliferation and/or stromal activation and angiogenesis through autocrine or paracrine loops with the appropriate receptor-bearing cells (Mueller et al 2001). There is no report on expression of growth factor granulocyte colony-stimulating factor (G-CSF) in the experimental model, colon adenocarcinoma cell line (Caco2), that is commonly used in drug permeability assays. We analyzed mRNA and protein expression of GCSF in Caco2 cells using reverse transcriptase-PCR and SDS-PAGE.

Results

Conclusion