title: Expression of the apoptosis-inducing ligands FasL and TRAIL in malignant and benign human breast tumors.
abstract: Apoptosis-inducing ligands such as Fas ligand (FasL) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) have been found to play an important role in cell regulation. Different malignant tumors show an altered expression of these ligands and their respective receptors compared to normal tissues. The purpose of this study was therefore to investigate expression of TRAIL, FasL, and its receptor Fas on protein and mRNA levels in breast carcinomas (n=40), fibroadenomas (n=7), and normal breast tissues (n=5). Immunohistochemical reaction demonstrated that FasL was strongly expressed in breast cancer tissues (34/40) while only one fibroadenoma and one normal breast tissue reacted weakly positive for FasL. All fibroadenomas and normal breast tissues as well as the majority of breast cancer tissues expressed Fas on protein level. Quantitative RT-PCR analysis detected high expression of FasL mRNA in breast cancer tissues and fibroadenomas, whereas fibroadenomas showed the highest Fas mRNA copy numbers, followed by breast cancer tissues and normal breast tissues (P<0.05). Compared to FasL expression, TRAIL could be detected in less breast cancer tissues on protein level (21/40) and was found in only one fibroadenoma and none of the normal breast tissues. Thus, it can be concluded that malignant breast tumors show an altered expression of the two apoptosis-inducing ligands FasL and TRAIL.
authors.affiliation: Department of Obstetrics and Gynecology, University of Rostock, Germany.
authors.forename: C
authors.initials: C
authors.lastname: Herrnring
authors.forename: T
authors.initials: T
authors.lastname: Reimer
authors.forename: U
authors.initials: U
authors.lastname: Jeschke
authors.forename: J
authors.initials: J
authors.lastname: Makovitzky
authors.forename: K
authors.initials: K
authors.lastname: Krüger
authors.forename: B
authors.initials: B
authors.lastname: Gerber
authors.forename: D
authors.initials: D
authors.lastname: Kabelitz
authors.forename: K
authors.initials: K
authors.lastname: Friese
mesh_terms: D017209:Apoptosis; D051017:Apoptosis Regulatory Proteins; D001940:Breast / Q000378:metabolism; D001943:Breast Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D053222:Fas Ligand Protein; D005260:Female; D018226:Fibroadenoma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D019084:Fluorescent Antibody Technique, Indirect; D015870:Gene Expression; D006801:Humans; D007124:Immunoenzyme Techniques; D008024:Ligands; D008562:Membrane Glycoproteins / Q000096:biosynthesis / Q000235:genetics*; D009363:Neoplasm Proteins / Q000096:biosynthesis / Q000235:genetics*; D012333:RNA, Messenger / Q000096:biosynthesis*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D053221:TNF-Related Apoptosis-Inducing Ligand; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics*; D019014:fas Receptor / Q000096:biosynthesis / Q000235:genetics
chemical_list: D051017:Apoptosis Regulatory Proteins; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008024:Ligands; D008562:Membrane Glycoproteins; D009363:Neoplasm Proteins; D012333:RNA, Messenger; D053221:TNF-Related Apoptosis-Inducing Ligand; C505653:TNFSF10 protein, human; D014409:Tumor Necrosis Factor-alpha; D019014:fas Receptor