Evidence map›Paper›PMID 25197352›Full record

ArticleInternational journal of clinical and experimental pathology2014

CBX8, a novel DNA repair protein, promotes tumorigenesis in human esophageal carcinoma.

Weifan Xiao, Chao Ou, Jinlong Qin, Feng Xing, Yi Sun, Zhi Li, Jin Qiu

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.7field-weighted citation impact, top 31% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 25 citations in OpenAlex.

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  9. Observational
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  14. The microRNA signatures: aberrantly expressed miRNAs in prostate cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2019
    Review
  15. Article
  16. Article
  17. CBX8 and CD96 Are Important Prognostic Biomarkers of Colorectal Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Weifan XiaoDepartment of Gynaecology and Obstetrics, Shanghai Tenth People's Hospital of Tongji University Shanghai 200072, China.
Chao OuDepartment of Clinical Laboratory, The Affiliated Tumor Hospital of Guangxi Medical University Nanning 530021, Guangxi Province, China.
Jinlong QinDepartment of Gynaecology and Obstetrics, Shanghai Tenth People's Hospital of Tongji University Shanghai 200072, China.
Feng XingDepartment of Gynaecology and Obstetrics, Shanghai Tenth People's Hospital of Tongji University Shanghai 200072, China.
Yi SunDepartment of Gynaecology and Obstetrics, Shanghai Tenth People's Hospital of Tongji University Shanghai 200072, China.
Zhi LiDepartment of Clinical Laboratory Medicine, Shanghai Yangpu District Central Hospital Shanghai 200433, China.
Jin QiuDepartment of Gynaecology and Obstetrics, Shanghai Tenth People's Hospital of Tongji University Shanghai 200072, China.
Shanghai Tenth People's Hospital · CNTumor Hospital of Guangxi Medical University · CNYangpu Hospital of Tongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA damage response and repair are carried out by certain proteins following damage by environmental clastogens, such as ionizing radiation and reactive oxygen species. It has been reported that many carcinomas that are characterized by resistance to chemotherapy and poor outcomes show dysfunction of these proteins. Chromobox homologue 8 (CBX8), a member of the polycomb group of proteins, has been identified as a factor that protects tumor cells from the detrimental effects of ionizing radiation (IR) or hydrogen peroxide (H2O2). In this study, we found that CBX8 was up-regulated in esophageal carcinoma tissues compared with adjacent non-cancerous tissues (P<0.01) and correlated with TNM stage in esophageal squamous cell carcinoma patients. Depletion of CBX8 decreased cell proliferation both in vitro and in vivo and increased the phosphorylation levels of p21, Wee1, and CHK1, which result in cyclin-dependent kinase inhibition and cell-cycle delay. CBX8 depletion also led to accumulation of spontaneous DNA damage and raised the sensitivity of tumor cells to IR or H2O2. We also found that the total level of CBX8 in the cells was increased after treating tumor cells with clastogens. In addition, our data showed that decreased CBX8 expression was accompanied by the reduction of EZH2 and EED, which have been reported to participate in DNA damage repair. Collectively, CBX8 might emerge as an oncogene for promoting the proliferation of tumor cells and raising the resistance of neoplasms to chemotherapy.

Indexed as

AnimalsBlotting, WesternCarcinogenesisCarcinoma, Squamous CellCell Line, TumorCell ProliferationDNA Repair EnzymesDrug Resistance, NeoplasmEsophageal NeoplasmsHeterograftsHumansImmunohistochemistryMiceMice, NudePolycomb Repressive Complex 1Real-Time Polymerase Chain ReactionCBX8 protein, humanDNA Repair EnzymesPolycomb Repressive Complex 1RNA, Small InterferingCBX8DNA repairesophageal carcinomaG2M cell cycletumorigenesis

Identifiers

PMID25197352
PMCPMC4152042
OpenAlexW1821205839

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.