PMID- 27756570
OWN - NLM
STAT- MEDLINE
DCOM- 20170731
LR  - 20171029
IS  - 1872-7980 (Electronic)
IS  - 0304-3835 (Linking)
VI  - 384
DP  - 2017 Jan 1
TI  - Epigenetic silencing of HOPX contributes to cancer aggressiveness in breast
      cancer.
PG  - 70-78
LID - S0304-3835(16)30629-2 [pii]
LID - 10.1016/j.canlet.2016.10.017 [doi]
AB  - Epigenetic silencing of HOPX has been shown to be frequent and specific in human 
      cancers. HOPX is thought as a tumor suppressor gene and its promoter methylation 
      is the main mechanism of down-regulation. In non-hereditary breast cancer, since 
      roles of epigenetic modifications are more critical than in other cancers, the
      aim of this study is to seek into the roles and clinical relevance of epigenetic 
      silencing of HOPX. Down-regulation of HOPX was observed in all human breast
      cancer cell lines tested. The promoter methylation was found in six of seven cell
      lines, and demethylating agents restored HOPX expression. The promoter
      methylation was cancer-specific in human breast tissues. Forced expression of
      HOPX attenuated anchorage-independent growth in vitro. HOPX promoter methylation 
      independently predicted worse prognosis of breast cancer patients. Of note, HOPX 
      promoter methylation was significantly associated with HER2 positivity as well as
      advanced lymph node metastasis. HOPX promoter methylation is not only frequent
      and cancer-specific but also associated with aggressive phenotype in breast
      cancer. Epigenetic silencing of HOPX may have clinical potential as a biomarker
      in the treatment strategy of breast cancer patients.
CI  - Copyright (c) 2016. Published by Elsevier Ireland Ltd.
FAU - Kikuchi, Mariko
AU  - Kikuchi M
AD  - Department of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
FAU - Katoh, Hiroshi
AU  - Katoh H
AD  - Department of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
FAU - Waraya, Mina
AU  - Waraya M
AD  - Department of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
FAU - Tanaka, Yoko
AU  - Tanaka Y
AD  - Department of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
FAU - Ishii, Satoru
AU  - Ishii S
AD  - Department of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
FAU - Tanaka, Toshimichi
AU  - Tanaka T
AD  - Department of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
FAU - Nishizawa, Nobuyuki
AU  - Nishizawa N
AD  - Department of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
FAU - Yokoi, Keigo
AU  - Yokoi K
AD  - Department of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
FAU - Minatani, Naoko
AU  - Minatani N
AD  - Department of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
FAU - Ema, Akira
AU  - Ema A
AD  - Department of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
FAU - Kosaka, Yoshimasa
AU  - Kosaka Y
AD  - Department of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
FAU - Tanino, Hirokazu
AU  - Tanino H
AD  - Department of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
FAU - Yamashita, Keishi
AU  - Yamashita K
AD  - Department of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
FAU - Watanabe, Masahiko
AU  - Watanabe M
AD  - Department of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
      Electronic address: intl-aff@kitasato-u.ac.jp.
LA  - eng
PT  - Journal Article
DEP - 20161015
PL  - Ireland
TA  - Cancer Lett
JT  - Cancer letters
JID - 7600053
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (HOP protein, human)
RN  - 0 (Homeodomain Proteins)
RN  - 0 (Tumor Suppressor Proteins)
RN  - EC 2.7.10.1 (ERBB2 protein, human)
RN  - EC 2.7.10.1 (Receptor, ErbB-2)
SB  - IM
MH  - Apoptosis
MH  - Biomarkers, Tumor/*genetics/metabolism
MH  - Breast Neoplasms/*genetics/metabolism/pathology
MH  - Cell Proliferation
MH  - *DNA Methylation
MH  - *Epigenesis, Genetic
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - *Gene Silencing
MH  - Homeodomain Proteins/*genetics/metabolism
MH  - Humans
MH  - Lymphatic Metastasis
MH  - MCF-7 Cells
MH  - Neoplasm Invasiveness
MH  - Phenotype
MH  - Prognosis
MH  - Promoter Regions, Genetic
MH  - Receptor, ErbB-2/metabolism
MH  - Time Factors
MH  - Transfection
MH  - Tumor Suppressor Proteins/*genetics/metabolism
OTO - NOTNLM
OT  - *Breast cancer
OT  - *Epigenetic silencing
OT  - *HER2
OT  - *HOPX
EDAT- 2016/10/28 06:00
MHDA- 2017/08/02 06:00
CRDT- 2016/11/07 06:00
PHST- 2016/02/10 00:00 [received]
PHST- 2016/10/06 00:00 [revised]
PHST- 2016/10/06 00:00 [accepted]
PHST- 2016/10/28 06:00 [pubmed]
PHST- 2017/08/02 06:00 [medline]
PHST- 2016/11/07 06:00 [entrez]
AID - S0304-3835(16)30629-2 [pii]
AID - 10.1016/j.canlet.2016.10.017 [doi]
PST - ppublish
SO  - Cancer Lett. 2017 Jan 1;384:70-78. doi: 10.1016/j.canlet.2016.10.017. Epub 2016
      Oct 15.