Effects of alpha fetoprotein on escape of Bel 7402 cells from attack of lymphocytes

Mengsen Li,Pingfeng Li,Sheng Zhou,Xinhua Liu,Gang Li

doi:10.1186/1471-2407-5-96

Mengsen Li, Pingfeng Li + Show 3 more

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https://doi.org/10.1186/1471-2407-5-96

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Journal: BMC Cancer	Publication Date: Aug 5, 2005
Citations: 62	License type: cc-by

Affiliation: Peking University, Hainan Medical College Hospital

Abstract

BackgroundInvolvement of AFP against apoptosis of tumor cell has been implicated in its evasion of immune surveillance. However, the molecular events of immune escape mechanisms are still unknown. The major observations reported here relate to a possible mechanism by which heptoloma Bel 7402 cells escape immune surveillance in vitro.MethodsWestern blotting and a well-characterized cofocal scanning image were performed to analyze the expression of Fas/FasL and caspase-3 in co-cultured Bel 7402 and Jurkat cells.ResultsAfter co-culture with Jurkat cells, up-regulated Fas and reduced FasL expression could be observed. Treatment with AFP could remarkably inhibit the elevated Fas and, whereas, induce the FasL expression in co-cultured Bel 7402 cells. Cells co-culture could induce the expression of caspase-3 in both cells line. The elevated caspase-3 in Bel 7402 cells was abolished following the treatment of AFP. The expression of caspase-3 was elevated in co-cultured Jurkat cells treated with AFP. No detectable change on the expression of survivin was examined in both cells line. Monoclonal antibody against AFP treatment alone did not obviously influence the growth of cells, as well as the expression of Fas/FasL and caspase-3. However, the effect of AFP could be blocked by antibody.Conclusionsour results provide evidence that AFP could promote the escape of liver cancer cells from immune surveillance through blocking the caspase signal pathway of tumor cells and triggering the Fas/FasL interaction between tumor cells and lymphocytes.

Highlights

Involvement of Alpha fetoprotein (AFP) against apoptosis of tumor cell has been implicated in its evasion of immune surveillance
Conclusions: our results provide evidence that AFP could promote the escape of liver cancer cells from immune surveillance through blocking the caspase signal pathway of tumor cells and triggering the Fas/FasL interaction between tumor cells and lymphocytes
The effects of AFP on the growth of co-cultured cells To observe the effects of AFP on the escape of Bel 7402 cells from the attack of lymphocytes, AFP at a concentration of 20 mg/L, which has been reported and proved to be an optimal dose according to the dose response curves in our recent experiments [unpublished data], was added into co-cultured cells

Summary

Introduction

Involvement of AFP against apoptosis of tumor cell has been implicated in its evasion of immune surveillance. The major observations reported here relate to a possible mechanism by which heptoloma Bel 7402 cells escape immune surveillance in vitro. Besides its role as a carrier or transporter for various serum ligands including fatty acids, retinoids, steroids, drugs, dyes and heavy metals, AFP has been reported to display growth regulatory properties. Multitude of cell types involving the growth and differentiation effects of AFP include placental [1], lymphoid [2], ovarian [3], uterine [4], gastric cancer [5], epidermal [6], breast cancer [7] and fetal fibroblasts [8]. Some studies on the mechanisms of AFP suggested that AFP (page number not for citation purposes)

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