Evidence map›Paper›PMID 22964637›Full record

ArticleOncogene2013

The tumor suppressor Caliban regulates DNA damage-induced apoptosis through p53-dependent and -independent activity.

Y Wang, Z Wang, B H Joshi, R K Puri, B Stultz, Q Yuan, Y Bai, P Zhou, Z Yuan, D A Hursh and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.1field-weighted citation impact, top 47% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

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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

11 authors at 5 institutions in 2 countries.

Y WangCAS Key Laboratory for Biological Effects of Nanomaterials and Nanosafety, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing, China.
Z Wang
B H Joshi
R K Puri
B Stultz
Q Yuan
Y Bai
P Zhou
Z Yuan
D A Hursh
X Bi
Center for Biologics Evaluation and Research · USChinese Academy of Sciences · CNBeijing Radiation Center · CNDalian Medical University · CNInstitute of High Energy Physics · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously identified Caliban (Clbn) as the Drosophila homolog of human Serologically defined colon cancer antigen 1 gene and demonstrated that it could function as a tumor suppressor in human non-small-cell lung cancer (NSCLC) cells, although its mode of action was unknown. Herein, we identify roles for Clbn in DNA damage response. We generate clbn knockout flies using homologous recombination and demonstrate that they have a heightened sensitivity to irradiation. We show that normal Clbn function facilitates both p53-dependent and -independent DNA damage-induced apoptosis. Clbn coordinates different apoptosis pathways, showing a two-stage upregulation following DNA damage. Clbn has proapoptotic functions, working with both caspase and the proapoptotic gene Hid. Finally, ecotopic expression of clbn(+) in NSCLC cells suppresses tumor formation in athymic nude mice. We conclude that Caliban is a regulator of DNA damage-induced apoptosis, functioning as a tumor suppressor in both p53-dependent and -independent pathways.

Indexed as

AnimalsApoptosisCarcinoma, Non-Small-Cell LungCell Line, TumorDNA DamageDrosophilaDrosophila ProteinsGene Knockout TechniquesHumansImmunohistochemistryMiceMice, NudeMicroscopy, ConfocalMicroscopy, Electron, ScanningNeoplasms, ExperimentalReverse Transcriptase Polymerase Chain ReactionClbn protein, DrosophilaDrosophila ProteinsTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID22964637
OpenAlexW2105841071

What OpenQuestion holds

Textmetadata
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.