Evidence map›Paper›PMID 23880825›Full record

ArticleBritish journal of cancer2013

The interaction between C35 and ΔNp73 promotes chemo-resistance in ovarian cancer cells.

T H-Y Leung, S C-S Wong, K K-L Chan, D W Chan, A N-Y Cheung, H Y-S Ngan

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. TAp73 represses NF-κB-mediated recruitment of tumor-associated macrophages in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  5. Article
  6. PRSS1 Upregulation Predicts Platinum Resistance in Ovarian Cancer Patients.Frontiers in cell and developmental biology · 2020
    Article
  7. Article
  8. Review
  9. Emerging targets in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2019
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Overexpression of the ∆Np73 isoform is associated with centrosome amplification in brain tumor cell lines.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  16. Review
  17. Oncogenes associated with drug resistance in ovarian cancer.Journal of cancer research and clinical oncology · 2015
    Review
  18. TAp73 suppresses tumor angiogenesis through repression of proangiogenic cytokines and HIF-1α activity.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  19. Article
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

6 authors at 1 institution in 1 country.

T H-Y LeungDepartment of Obstetrics and Gynaecology, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region.
S C-S Wong
K K-L Chan
D W Chan
A N-Y Cheung
H Y-S Ngan
University of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe purpose of this study was to characterise the oncogenic roles of C35, a novel protein binding partner of ΔNp73, in ovarian cancer and to investigate the functional significance of C35-ΔNp73 interaction in the regulation of chemo-resistance.

methodsC35 expression was evaluated by quantitative real-time PCR in human ovarian cancer tissues and cell lines. The aggressiveness of ovarian cancer cells overexpressing C35 was examined by cell proliferation, migration, soft agar and nude mouse xenograft. The significance of C35-ΔNp73 interaction in chemo-resistance was evaluated by apoptosis assays and cell viability after cisplatin treatment.

resultsThe expression of C35 was significantly enhanced in human ovarian cancer tissues. Overexpression of C35 augmented proliferation, migration and tumourigenicity in ovarian cancer cell lines. C35 knockdown inhibited cell motility and cell growth. The co-expression of C35 and ΔNp73 by transient or stable transfection in ovarian cancer cells induced greater resistance to cisplatin treatment than did transfection with C35 or ΔNp73 alone. The cisplatin resistance was demonstrated to be caused by increased AKT and NFκB activity induced by C35-ΔNp73.

conclusionOur results suggest that ΔNp73 might cooperate with C35 to promote tumour progression and contribute to cisplatin resistance in ovarian cancer cells. Future studies of the functional roles of ΔNp73 and C35 will provide insight that will aid in the establishment of new strategies and more effective therapies.

Indexed as

Antineoplastic AgentsCisplatinAnimalsCell Line, TumorDNA-Binding ProteinsDrug Resistance, NeoplasmFemaleHumansIntracellular Signaling Peptides and ProteinsMiceMice, NudeNeoplasm ProteinsNF-kappa BNuclear ProteinsOvarian NeoplasmsProto-Oncogene Proteins c-aktAntineoplastic AgentsCisplatindelta Np73 protein, humanDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsMIEN1 protein, humanNeoplasm ProteinsNF-kappa BNuclear ProteinsProto-Oncogene Proteins c-aktTrp73 protein, mouseTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID23880825
PMCPMC3749569
OpenAlexW2034348592

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.