title: Specific killing of CCR9 high-expressing acute T lymphocytic leukemia cells by CCL25 fused with PE38 toxin.
abstract: We have previously demonstrated that CCR9 plays a pivotal role in drug resistance and invasion in human acute T-lymphocytic leukemia (T-ALL). In this study, we investigated whether the MOLT4 cells, which naturally express CCR9 at high levels, can be successfully killed by the specific ligand, CCL25 fused to Pseudomonas exotoxin 38 (PE38) toxin. Our results demonstrated that CCL25-PE38 was able to specifically kill MOLT4 cells via apoptosis induction, and suppress the growth of CCR9(+) tumors. This work shows that CCR9 high-expressing human T-ALL cells can be successfully killed by delivering PE38 toxin fused to the ligand CCL25.
authors.affiliation: Department of Immunology, School of Basic Medical Science, Wuhan University, Wuchang, Wuhan, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Hu
authors.forename: Li
authors.initials: L
authors.lastname: Zhang
authors.forename: Ranran
authors.initials: R
authors.lastname: Wu
authors.forename: Rongfei
authors.initials: R
authors.lastname: Han
authors.forename: Yanhan
authors.initials: Y
authors.lastname: Jia
authors.forename: Zhengming
authors.initials: Z
authors.lastname: Jiang
authors.forename: Mengxin
authors.initials: M
authors.lastname: Cheng
authors.forename: Jing
authors.initials: J
authors.lastname: Gan
authors.forename: Xiang
authors.initials: X
authors.lastname: Tao
authors.forename: Qiuping
authors.initials: Q
authors.lastname: Zhang
mesh_terms: D036002:ADP Ribose Transferases / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D001427:Bacterial Toxins / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D002478:Cells, Cultured; D019742:Chemokines, CC / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D004353:Drug Evaluation, Preclinical; D005098:Exotoxins / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D051379:Mice; D016513:Mice, SCID; D054218:Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / Q000188:drug therapy* / Q000473:pathology*; D054388:Receptors, CCR / Q000378:metabolism*; D011993:Recombinant Fusion Proteins / Q000494:pharmacology / Q000627:therapeutic use; D013379:Substrate Specificity; D037521:Virulence Factors / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D023041:Xenograft Model Antitumor Assays; D000097668:Pseudomonas aeruginosa Exotoxin A
chemical_list: D036002:ADP Ribose Transferases; D001427:Bacterial Toxins; D019742:Chemokines, CC; D005098:Exotoxins; D054388:Receptors, CCR; D011993:Recombinant Fusion Proteins; D037521:Virulence Factors; D000097668:Pseudomonas aeruginosa Exotoxin A; C119309:CC chemokine receptor 9; C108074:CCL25 protein, human