title: CMTM8 is Frequently Downregulated in Multiple Solid Tumors.
abstract: Previous studies have demonstrated that overexpression of CMTM8 inhibits cell growth and induces apoptosis in multiple types of cancer cells, whereas the downregulation of CMTM8 induces the epithelial-to-mesenchymal (EMT)-like phenotype in hepatocyte carcinoma cells, implying its important roles in tumorigenesis and tumor metastasis. No extensive studies on the expression of CMTM8 in either normal or tumorous human tissues have been reported to date. Here, using real-time quantitative polymerase chain reaction, we analyzed CMTM8 expression in multiple normal human tissue samples. Moreover, by applying high-throughput immunohistochemical staining of tissue microarrays with homemade anti-CMTM8 antibodies, we studied CMTM8 expression in carcinoma samples and adjacent normal samples of 6 types of human tissues. CMTM8 is widely expressed in many normal human tissues and is frequently downregulated or absent in multiple solid tumors (liver, lung, colon, rectum, esophagus, stomach). χ tests revealed a significant negative correlation between CMTM8 expression and tumorigenesis: liver, lung (squamous carcinoma), colon, rectum, P<0.0001; esophagus, P<0.001; stomach, P<0.01. Real-time quantitative polymerase chain reaction analysis of samples from esophageal carcinomas and the adjacent normal tissues revealed that CMTM8 mRNA levels are reduced in carcinomas compared with normal tissues, indicating that CMTM8 is potentially downregulated at the mRNA level (P<0.01). This is the first extensive study of CMTM8 expression in both normal and tumorous human tissues. Our findings strongly supported the potential role of CMTM8 as a novel tumor suppressor and may shape further functional studies on this gene.
authors.affiliation: *Department of Immunology, School of Basic Medical Sciences, Key Laboratory of Immunology, Ministry of Health, Peking University Health Science Center †National Institutes for Food and Drug Control ‡Peking University People's Hospital, Beijing, P.R. China.
authors.forename: Wenjuan
authors.initials: W
authors.lastname: Zhang
authors.forename: Hui
authors.initials: H
authors.lastname: Qi
authors.forename: Xiaoning
authors.initials: X
authors.lastname: Mo
authors.forename: Qianying
authors.initials: Q
authors.lastname: Sun
authors.forename: Ting
authors.initials: T
authors.lastname: Li
authors.forename: Quansheng
authors.initials: Q
authors.lastname: Song
authors.forename: Kexin
authors.initials: K
authors.lastname: Xu
authors.forename: Hao
authors.initials: H
authors.lastname: Hu
authors.forename: Dalong
authors.initials: D
authors.lastname: Ma
authors.forename: Ying
authors.initials: Y
authors.lastname: Wang
mesh_terms: D018925:Chemokines / Q000235:genetics / Q000378:metabolism*; D015536:Down-Regulation; D006367:HeLa Cells; D056945:Hep G2 Cells; D006801:Humans; D007150:Immunohistochemistry; D062792:MARVEL Domain-Containing Proteins / Q000235:genetics / Q000378:metabolism*; D009369:Neoplasms / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics
chemical_list: C507076:CMTM8 protein, human; D018925:Chemokines; D062792:MARVEL Domain-Containing Proteins; D012333:RNA, Messenger