title: Aberrant expression of CKLF-like MARVEL transmembrane member 5 (CMTM5) by promoter methylation in myeloid leukemia.
abstract: CMTM5 has been shown to exhibit tumor suppressor activities, however, its role in leukemia is unclear. Herein we firstly reported the expression and function of CMTM5 in myeloid leukemia. CMTM5 was down-regulated, or undetectable, in leukemia cell lines and bone marrow cells from leukemia patients with promoter methylation. Ectopic expression of CMTM5-v1 strongly inhibited the proliferation of K562 and MEG-01 cells. In addition, significant negative correlations were observed between CMTM5 and three leukemia-specific fusion genes (AML1-ETO, PML-RARα and BCR/ABL1). CMTM5 expression was up-regulated in patients who had undergone treatment. Therefore, CMTM5 may be involved in the pathomechanism of myeloid leukemias.
authors.affiliation: Peking University People's Hospital and Institute of Hematology, Beijing, China.
authors.forename: Jihong
authors.initials: J
authors.lastname: Niu
authors.forename: Henan
authors.initials: H
authors.lastname: Li
authors.forename: Yao
authors.initials: Y
authors.lastname: Zhang
authors.forename: Jinlan
authors.initials: J
authors.lastname: Li
authors.forename: Min
authors.initials: M
authors.lastname: Xie
authors.forename: Lingdi
authors.initials: L
authors.lastname: Li
authors.forename: Xiaoying
authors.initials: X
authors.lastname: Qin
authors.forename: Yazhen
authors.initials: Y
authors.lastname: Qin
authors.forename: Xiaohuan
authors.initials: X
authors.lastname: Guo
authors.forename: Qian
authors.initials: Q
authors.lastname: Jiang
authors.forename: Yanrong
authors.initials: Y
authors.lastname: Liu
authors.forename: Shanshan
authors.initials: S
authors.lastname: Chen
authors.forename: Xiaojun
authors.initials: X
authors.lastname: Huang
authors.forename: Wenling
authors.initials: W
authors.lastname: Han
authors.forename: Guorui
authors.initials: G
authors.lastname: Ruan
mesh_terms: D000328:Adult; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D015153:Blotting, Western; D001854:Bone Marrow Cells / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D018925:Chemokines / Q000235:genetics* / Q000378:metabolism; D050676:Core Binding Factor Alpha 2 Subunit / Q000235:genetics; D019175:DNA Methylation; D015536:Down-Regulation; D005260:Female; D016044:Fusion Proteins, bcr-abl / Q000235:genetics; D015973:Gene Expression Regulation, Leukemic; D018922:HL-60 Cells; D006801:Humans; D020014:K562 Cells; D015470:Leukemia, Myeloid, Acute / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D062792:MARVEL Domain-Containing Proteins; D008297:Male; D015514:Oncogene Proteins, Fusion / Q000235:genetics; D011401:Promoter Regions, Genetic / Q000235:genetics*; D000075142:RUNX1 Translocation Partner 1 Protein; D012074:Remission Induction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D025521:Tumor Suppressor Proteins / Q000235:genetics* / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects; D055815:Young Adult
chemical_list: C107844:AML1-ETO fusion protein, human; C525020:CMTM5 protein, human; D018925:Chemokines; D050676:Core Binding Factor Alpha 2 Subunit; D062792:MARVEL Domain-Containing Proteins; D015514:Oncogene Proteins, Fusion; D000075142:RUNX1 Translocation Partner 1 Protein; D025521:Tumor Suppressor Proteins; C093476:promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; D016044:Fusion Proteins, bcr-abl