Evidence map›Paper›PMID 17179983›Full record

ArticleBritish journal of cancer2007

Elevated Bmi-1 expression is associated with dysplastic cell transformation during oral carcinogenesis and is required for cancer cell replication and survival.

M K Kang, R H Kim, S J Kim, F K Yip, K-H Shin, G P Dimri, R Christensen, T Han, N-H Park

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

72 citing papers in PubMed, 173 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. The Role of Polycomb Group Protein BMI1 in DNA Repair and Genomic Stability.International journal of molecular sciences · 2021
    Review
  11. Review
  12. Curcumin Derivative C086 Combined with Cisplatin Inhibits Proliferation of Osteosarcoma Cells.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  13. Article
  14. Observational
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

12 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 1 country.

M K KangUCLA School of Dentistry, Los Angeles, CA 90095, USA. mkang@dent.ucla.edu
R H Kim
S J Kim
F K Yip
K-H Shin
G P Dimri
R Christensen
T Han
N-H Park
University of California, Los Angeles · USNorthwestern University · USUCLA Jonsson Comprehensive Cancer Center

Funding

HPV, Genetic Instability &Oral CancerR01DE014147 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PARK, NO-HEE · 2001 to 2005
$1.2M
Combined Effect on HIV and HPV in Oral CancerK08DE017121 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KIM, REUBEN HAN-KYU · 2007 to 2011
$571k
Oxidative Stress, DNA Damage, and Cellular AgingK22DE015316 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KANG, MO KWAN · 2003 to 2006
$540k
NIDCR NIH HHS DE14147NIDCR NIH HHS DE15316NIDCR NIH HHS K08 DE017121NIDCR NIH HHS K22 DE015316NIDCR NIH HHS R01 DE014147
6 · The paper itself

Abstract

Bmi-1 is a polycomb group protein that was identified as c-myc cooperating oncogene in murine lymphomagenesis. The current study was undertaken to determine the role of Bmi-1 in human oral carcinogenesis. Bmi-1 protein and RNA expression levels were markedly enhanced in the cells of oral squamous cell carcinomas (OSCC) compared with that of normal human oral keratinocytes (NHOK). Enhanced-Bmi-1 expression was also detected in situ in the archived oral mucosal tissues with cancerous and precancerous histopathology, including that of mild epithelial dysplasia. Thus, Bmi-1 expression occurs at a very early stage in oral carcinogenesis. To determine the biological role of Bmi-1 in cell proliferation, endogenous Bmi-1 was knocked down in actively proliferating SCC4 cells and NHOK by RNA interference. After Bmi-1 knockdown, cell replication was severely retarded. However, the expression of p16(INK4A), a known cellular target of Bmi-1, was not changed in cells with or without Bmi-1 knockdown. Furthermore, Bmi-1 knockdown in HOK-16B-BaP-T cells, in which the p16(INK4A)/pRb pathway was abrogated, led to immediate arrest of replication and loss of viable cells. Thus, our data suggest that Bmi-1 may act through p16(INK4A)-independent pathways to regulate cellular proliferation during oral cancer progression.

Indexed as

Gene Expression ProfilingGene Expression Regulation, NeoplasticCarcinoma, Squamous CellCell LineCell ProliferationCell SurvivalCell Transformation, NeoplasticGene AmplificationHumansImmunohistochemistryKeratinocytesMouth NeoplasmsNuclear ProteinsPolycomb Repressive Complex 1Proto-Oncogene ProteinsRepressor ProteinsBMI1 protein, humanNuclear ProteinsPolycomb Repressive Complex 1Proto-Oncogene ProteinsRepressor ProteinsRNA, Messenger

Identifiers

PMID17179983
PMCPMC2360223
OpenAlexW2053434870

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.