Epigenetic silencing of HOPX contributes to cancer aggressiveness in breast cancer

Cancer Letters

Volumn 384, Issue , 2017, Pages 70-78

  Kikuchi, Mariko ^a   Katoh, Hiroshi ^a   Waraya, Mina ^a   Tanaka, Yoko ^a   Ishii, Satoru ^a   Tanaka, Toshimichi ^a   Nishizawa, Nobuyuki ^a   Yokoi, Keigo ^a   Minatani, Naoko ^a   Ema, Akira ^a   Kosaka, Yoshimasa ^a   Tanino, Hirokazu ^a   Yamashita, Keishi ^a   Watanabe, Masahiko ^a  

^a KITASATO UNIVERSITY SCHOOL OF MEDICINE   (Japan)

Author keywords

Breast cancer; Epigenetic silencing; HER2; HOPX

Indexed keywords

EPIDERMAL GROWTH FACTOR RECEPTOR 2; MEMBRANE PROTEIN; MESSENGER RNA; PROTEIN HOPX BETA; UNCLASSIFIED DRUG; ERBB2 PROTEIN, HUMAN; HOMEODOMAIN PROTEIN; HOP PROTEIN, HUMAN; TUMOR MARKER; TUMOR SUPPRESSOR PROTEIN;

ANCHORAGE INDEPENDENT GROWTH; ARTICLE; BREAST CANCER; BREAST CANCER CELL LINE; CANCER AGGRESSIVENESS; CANCER GROWTH; CANCER PATIENT; CANCER PROGNOSIS; CANCER STAGING; CELL PROLIFERATION; CONTROLLED STUDY; CPG ISLAND; DNA METHYLATION; DNA STRUCTURE; DOWN REGULATION; EPIGENETICS; GENE; GENE EXPRESSION REGULATION; GENE SILENCING; GENETIC ASSOCIATION; HOPX GENE; HUMAN; HUMAN CELL; HUMAN TISSUE; IMMUNOCYTOCHEMISTRY; IN VITRO STUDY; LYMPH NODE METASTASIS; MAJOR CLINICAL STUDY; ONCOLOGICAL PARAMETERS; PHENOTYPE; PREDICTIVE VALUE; PRIORITY JOURNAL; PROMOTER REGION; TRANSCRIPTION REGULATION; APOPTOSIS; BREAST TUMOR; FEMALE; GENETIC EPIGENESIS; GENETIC TRANSFECTION; GENETICS; MCF-7 CELL LINE; METABOLISM; PATHOLOGY; PROGNOSIS; TIME FACTOR; TUMOR INVASION;

APOPTOSIS; BIOMARKERS, TUMOR; BREAST NEOPLASMS; CELL PROLIFERATION; DNA METHYLATION; EPIGENESIS, GENETIC; FEMALE; GENE EXPRESSION REGULATION, NEOPLASTIC; GENE SILENCING; HOMEODOMAIN PROTEINS; HUMANS; LYMPHATIC METASTASIS; MCF-7 CELLS; NEOPLASM INVASIVENESS; PHENOTYPE; PROGNOSIS; PROMOTER REGIONS, GENETIC; RECEPTOR, ERBB-2; TIME FACTORS; TRANSFECTION; TUMOR SUPPRESSOR PROTEINS;

EID: 84992524643     PISSN: 03043835     EISSN: 18727980     Source Type: Journal    
DOI: 10.1016/j.canlet.2016.10.017     Document Type: Article

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