ArticleScientific reports2017
Brother of Regulator of Imprinted Sites (BORIS) suppresses apoptosis in colorectal cancer.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Atractyloside inhibits gefitinib‑resistant non‑small‑cell lung cancer cell proliferation.Oncology letters · 2024Article
- Cancer testis antigens: Emerging therapeutic targets leveraging genomic instability in cancer.Molecular therapy. Oncology · 2024Review
- Synaptopodin-2: a potential tumor suppressor.Cancer cell international · 2023Review
- Boris knockout eliminates AOM/DSS-induced in situ colorectal cancer by suppressing DNA damage repair and inflammation.Cancer science · 2023Article
- BTApep-TAT peptide inhibits ADP-ribosylation of BORIS to induce DNA damage in cancer.Molecular cancer · 2022Article
- 3D chromatin architecture and transcription regulation in cancer.Journal of hematology & oncology · 2022Review
- CTCFL regulates the PI3K-Akt pathway and it is a target for personalized ovarian cancer therapy.NPJ systems biology and applications · 2022Article
- Immunoprotective effect of an in silico designed multiepitope cancer vaccine with BORIS cancer-testis antigen target in a murine mammary carcinoma model.Scientific reports · 2021Article
- Brother of regulator of imprinted sites inhibits cisplatin-induced DNA damage in non-small cell lung cancer.Oncology letters · 2020Article
- BORIS/CTCFL promotes a switch from a proliferative towards an invasive phenotype in melanoma cells.Cell death discovery · 2020Article
- Atractyloside mimicsInternational journal of clinical and experimental pathology · 2018Article
- Intragenic DNA methylation and BORIS-mediated cancer-specific splicing contribute to the Warburg effect.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Long Non-Coding RNA Reprogramming (ROR) Promotes Cell Proliferation in Colorectal Cancer via Affecting P53.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 (H
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