title: Cytotoxicity Effects of Mouse IgG Produced against Three Nanoliposomal Human DR5 Receptor Epitopes on Breast Cancer Cells.
abstract: Cancer causes cells to avoid death while being the second cause of death in the world itself. Damaged cells in the absence of apoptosis will increasingly amplify their inefficient genome. Of the two main apoptosis inducing pathways in cells, the first has p53 protein as the main initiating factor in the cascade. According to research results this protein s mutated in 50% of cancers and sointerest has cooncentrated on the second pathway that features death receptors. Among these receptors TRAIL1/DR5 is especially expressed in cancer cells. So targeting such receptors can initiate the apoptotic cascade in cells. Interestingly by substitution of activating ligands with antibodies as agonists, we could efficiently turn on the apoptosis pathway. First of all, three small peptides from the DR5 protein extracellular domain were synthesized and injected with two different kind of adjuvants (Fround and liposomal encapsulation) separately into mice at 15 day intervals. As a result, liposomal peptides induced the immune system more efficient than Frounds adjuvant and at the end point the antibodies which were obtained from liposomal peptide injection induced much more effective death. Liposomal formol could be used as an adjuvant in immunization utilizing small peptides. They carry, protect and deliver peptides very efficiently. In addition, small peptides of a certain size from the extracellular domain of DR5 proteins not only can induce immune system but also produce antibodies playing a remarkable anti-cancer roles against breast cancer cells (MCF-7).
authors.affiliation: Department of Genetics, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran E-mail: dehghanih@yahoo.com and mhashemi@iautmu.ac.ir.
authors.forename: Shaghayegh
authors.initials: S
authors.lastname: Amirijavid
authors.forename: Maliheh
authors.initials: M
authors.lastname: Entezari
authors.forename: Abolfazl
authors.initials: A
authors.lastname: Movafagh
authors.forename: Mehrdad
authors.initials: M
authors.lastname: Hashemi
authors.forename: Alireza
authors.initials: A
authors.lastname: Mosavi-Jarahi
authors.forename: Hossein
authors.initials: H
authors.lastname: Dehghani
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D001943:Breast Neoplasms / Q000188:drug therapy / Q000276:immunology / Q000473:pathology*; D049109:Cell Proliferation / Q000187:drug effects; D004797:Enzyme-Linked Immunosorbent Assay; D000939:Epitopes / Q000276:immunology*; D005260:Female; D006801:Humans; D007114:Immunization; D007074:Immunoglobulin G / Q000276:immunology / Q000494:pharmacology*; D008081:Liposomes / Q000008:administration & dosage* / Q000737:chemistry; D051379:Mice; D008807:Mice, Inbred BALB C; D053758:Nanoparticles / Q000008:administration & dosage* / Q000737:chemistry; D010446:Peptide Fragments / Q000276:immunology; D053220:Receptors, TNF-Related Apoptosis-Inducing Ligand / Q000276:immunology*; D014407:Tumor Cells, Cultured
chemical_list: D000939:Epitopes; D007074:Immunoglobulin G; D008081:Liposomes; D010446:Peptide Fragments; D053220:Receptors, TNF-Related Apoptosis-Inducing Ligand