ArticleOncology reports2012
53BP1 suppresses tumor growth and promotes susceptibility to apoptosis of ovarian cancer cells through modulation of the Akt pathway.
Article in Oncology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Fallopian tubal histogenesis of ovarian endometriosis-A study of folate receptor-alpha expression.Frontiers in medicine · 2023Article
- Review
- Human iPSC-derived fallopian tube organoids with BRCA1 mutation recapitulate early-stage carcinogenesis.Cell reports · 2021Article
- RIF1 Links Replication Timing with Fork Reactivation and DNA Double-Strand Break Repair.International journal of molecular sciences · 2021Review
- Design and Construction of a Focused DNA-Encoded Library for Multivalent Chromatin Reader Proteins.Molecules (Basel, Switzerland) · 2020Article
- MicroRNA-23a depletion promotes apoptosis of ovarian cancer stem cell and inhibits cell migration by targeting DLG2.Cancer biology & therapy · 2019Article
- 53BP1 inhibits the migration and regulates the chemotherapy resistance of ovarian cancer cells.Oncology letters · 2018Article
- DNA repair genes PAXIP1 and TP53BP1 expression is associated with breast cancer prognosis.Cancer biology & therapy · 2017Article
- A central role of TRAX in the ATM-mediated DNA repair.Oncogene · 2016Article
- Expression of DNA damage checkpoint 53BP1 is correlated with prognosis, cell proliferation and apoptosis in colorectal cancer.International journal of clinical and experimental pathology · 2015Article
- Integration analysis of microRNA and mRNA expression profiles in human peripheral blood lymphocytes cultured in modeled microgravity.BioMed research international · 2014Article
- Role of 53BP1 in the regulation of DNA double-strand break repair pathway choice.Radiation research · 2014Review
- 53BP1 is a novel regulator of angiogenesis in breast cancer.Cancer science · 2013Article
- 53BP1 sensitizes breast cancer cells to 5-fluorouracil.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
53BP1 has been extensively studied as a key component of the DNA damage response, but little is known regarding the role of 53BP1 in preventing tumor development. The present study was designed to assess the impact of the modification of 53BP1 gene expression on the biological behavior of ovarian cancer cell lines and to elucidate the cellular pathway(s) triggered by 53BP1 in cancer cells. DNA liposome transfection technology was employed to increase and to knock down the expression of 53BP1 in A2780 and HO-8910PM cells, respectively. Viability, clonogenicity and cell cycle profiles were evaluated. Cell apoptosis was analyzed using flow cytometric assay. The expression of proteins related to apoptosis and cell signal transduction was assessed using western blotting. Increased expression of 53BP1 decreased the viability and the clonogenicity, and induced G₂/M arrest and apoptosis of the treated cells. The protein expression of Bax, P21 and caspase-3 was upregulated, while the levels of Bcl-2 and p-Akt were reduced to a statistically significant level. In contrast, deregulation of 53BP1 significantly increased proliferative ability. Collectively, our data suggest that 53BP1 is involved in several important steps in controlling cell proliferation and growth and preventing tumor development.
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Registered trials
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