title: Aberrant expression of HOX genes in human invasive breast carcinoma.
abstract: HOX genes are known not only as master genes that control the morphogenesis, but also as regulator genes that maintain tissue or organ specificity in the adult body. We hypothesized that dysregulated expression of HOX genes was associated with tumor development and malignant progression such as invasion and metastasis. In this study, we analyzed the expression patterns of 39 HOX genes in human invasive ductal breast cancer tissues and normal tissues by the real-time RT-PCR method. We found 11 HOX genes (HOXA1, A2, A3, A5, A9, C11, D3, D4, D8, D9 and D10) expression levels of which were significantly different between cancerous and normal tissues. All 10 genes except HOXC11 were expressed at lower levels in cancerous tissues than normal tissues. Comparing expression levels of each HOX gene among the different types of cancer tissues, the expression level of HOXB7 was lower in lymph node metastasis-positive cancer tissues than negative cancer tissues; those of HOXD12 and D13 were higher in progesterone receptor-positive cancer tissues than negative cancer tissues; and the expression level of HOXC5 was lower in cancerous tissues with mutated-type p53 than in normal and cancerous tissues with wild-type p53. These results suggest that the aberrant expression of HOX genes is related to the development of breast cancer and malignant behavior of cancer cells.
authors.affiliation: Division of Cancer-Related Genes, Institute for Genetic Medicine, Hokkaido University, Kita-15, Nishi-7, Kita-ku, Sapporo 060-0815, Japan.
authors.forename: Kokonoe
authors.initials: K
authors.lastname: Makiyama
authors.forename: Jun-Ichi
authors.initials: J
authors.lastname: Hamada
authors.forename: Minoru
authors.initials: M
authors.lastname: Takada
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Murakawa
authors.forename: Yoko
authors.initials: Y
authors.lastname: Takahashi
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Tada
authors.forename: Eiji
authors.initials: E
authors.lastname: Tamoto
authors.forename: Gaku
authors.initials: G
authors.lastname: Shindo
authors.forename: Akihiro
authors.initials: A
authors.lastname: Matsunaga
authors.forename: Ken-Ichi
authors.initials: K
authors.lastname: Teramoto
authors.forename: Kazuteru
authors.initials: K
authors.lastname: Komuro
authors.forename: Satoshi
authors.initials: S
authors.lastname: Kondo
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Katoh
authors.forename: Takao
authors.initials: T
authors.lastname: Koike
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Moriuchi
mesh_terms: D000328:Adult; D000368:Aged; D001940:Breast / Q000473:pathology; D001943:Breast Neoplasms / Q000378:metabolism* / Q000473:pathology; D002277:Carcinoma / Q000378:metabolism*; D045744:Cell Line, Tumor; D016000:Cluster Analysis; D018450:Disease Progression; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D005801:Genes, Homeobox / Q000235:genetics*; D006801:Humans; D008207:Lymphatic Metastasis; D008875:Middle Aged; D009154:Mutation; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D012313:RNA / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D016159:Tumor Suppressor Protein p53; D012313:RNA