title: Brother of Regulator of Imprinted Sites (BORIS) suppresses apoptosis in colorectal cancer.
abstract: Identifying oncogenes that promote cancer cell proliferation or survival is critical for treatment of colorectal cancer. The Brother of Regulator of Imprinted Sites (BORIS) is frequently expressed in most types of cancer, but rarely in normal tissues. Aberrantly expressed BORIS relates to colorectal cancer, but its function in colorectal cancer cells remains unclear. In addition, previous studies indicated the significance of cytoplasm-localized BORIS in cancer cells. However, none of them investigated its function. Herein, we investigated the functions of BORIS in cancer cell proliferation and apoptosis and the role of cytoplasm-localized BORIS in colorectal cancer. BORIS expression correlated with colorectal cancer proliferation. BORIS overexpression promoted colorectal cancer cell growth, whereas BORIS knockdown suppressed cell proliferation. Sensitivity of colorectal cancer cells to 5-fluorouracil (5-FU) was inversely correlated with BORIS expression. These data suggest that BORIS functions as an oncogene in colorectal cancer. BORIS silencing induced reactive oxygen species (ROS) production and apoptosis, whereas BORIS supplementation inhibited apoptosis induced by BORIS short interfering RNA (siRNA), hydrogen peroxide (H2O2) or 5-FU. Introduction of BORIS-ZFdel showed that cytoplasmic localization of BORIS inhibited apoptosis but not ROS production. Our study highlights the anti-apoptotic function of BORIS in colorectal cancer.
authors.affiliation: Center for Molecular Medicine, Zhejiang Academy of Medical Science, Hangzhou, Zhejiang Province, 310012, P.R. China.
authors.forename: Yanmei
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Center for Molecular Medicine, Zhejiang Academy of Medical Science, Hangzhou, Zhejiang Province, 310012, P.R. China.
authors.forename: Mengdie
authors.initials: M
authors.lastname: Fang
authors.affiliation: Center for Molecular Medicine, Zhejiang Academy of Medical Science, Hangzhou, Zhejiang Province, 310012, P.R. China.
authors.forename: Yongfei
authors.initials: Y
authors.lastname: Song
authors.affiliation: Center for Molecular Medicine, Zhejiang Academy of Medical Science, Hangzhou, Zhejiang Province, 310012, P.R. China.
authors.forename: Juan
authors.initials: J
authors.lastname: Ren
authors.affiliation: Center for Molecular Medicine, Zhejiang Academy of Medical Science, Hangzhou, Zhejiang Province, 310012, P.R. China.
authors.forename: Jianfei
authors.initials: J
authors.lastname: Fang
authors.affiliation: Center for Molecular Medicine, Zhejiang Academy of Medical Science, Hangzhou, Zhejiang Province, 310012, P.R. China.
authors.forename: Xiaoju
authors.initials: X
authors.lastname: Wang
mesh_terms: D000368:Aged; D017209:Apoptosis / Q000235:genetics; D002453:Cell Cycle / Q000235:genetics; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D002470:Cell Survival / Q000235:genetics; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D005260:Female; D005472:Fluorouracil / Q000494:pharmacology; D015972:Gene Expression Regulation, Neoplastic; D020868:Gene Silencing; D016259:Genes, myc; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009367:Neoplasm Staging; D021381:Protein Transport; D034741:RNA, Small Interfering / Q000235:genetics; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: C456540:CTCFL protein, human; D004268:DNA-Binding Proteins; D034741:RNA, Small Interfering; D017382:Reactive Oxygen Species; D005472:Fluorouracil