Evidence map›Paper›PMID 12768191›Full record

ArticleCancer gene therapy2003

Endogenous p21WAF1/CIP1 status predicts the response of human tumor cells to wild-type p53 and p21WAF1/CIP1 overexpression.

Marijeta Kralj, Koraljka Husnjak, Tajana Körbler, Jasminka Pavelić

Abstract read
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In one paragraph

Article in Cancer gene therapy, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 30 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

4 authors at 1 institution in 1 country.

Marijeta KraljDivision of Molecular Medicine, Rudjer Bosković Institute, Bijenicka c. 54, HR-10002 Zagreb, Croatia. mhorvat@rudjer.irb.hr
Koraljka Husnjak
Tajana Körbler
Jasminka Pavelić
Rudjer Boskovic Institute · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Expression of exogenous wild-type (wt) p53 protein can suppress the growth and/or induce apoptosis in different tumor cells. The effect of exogenous p21(WAF1/CIP1) expression is more controversial: while it can induce apoptosis in some cells, it can protect against p53-mediated apoptosis in others. We used adenoviral vectors to introduce p53 and p21(WAF1/CIP1) genes into human tumor cell lines with different p53 and/or p21(WAF1/CIP1) status. The cell growth inhibition and the induction of apoptosis were measured. Overexpression of wt p53 induced more efficient growth inhibition and apoptosis in SW 620 (mutant p53) and HeLa (inactivated p53 protein) than in MCF-7 (wt p53) and CaCo-2 cell line, which was the most resistant to p53 overexpression despite the p53 mutation. Unlike HeLa and SW 620 cells, the basal p21 protein level was readily detected in CaCo-2 and MCF-7 cells. Overexpression of p21(WAF1/CIP1) gene induced somewhat less pronounced growth inhibition of all cell lines tested, but it also induced apoptosis in HeLa and SW 620 cells. These results suggest that the basal, but not the inducible, levels of p21(WAF1/CIP1) protein in tumor cells could protect from p53-mediated apoptosis. On the other hand, overexpression of p21(WAF1/CIP1) gene itself can induce apoptosis in cells with no basal p21(WAF1/CIP1) protein level. Possible mechanisms of the differential response to these genes are discussed.

Indexed as

ApoptosisGenes, p53AdenoviridaeCell DivisionCell Line, TumorCyclin-Dependent Kinase Inhibitor p21CyclinsDNA FragmentationGenetic TherapyHeLa CellsHumansImmunohistochemistryMutationNeoplasmsReverse Transcriptase Polymerase Chain ReactionTime FactorsCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21CyclinsTumor Suppressor Protein p53

Identifiers

PMID12768191
OpenAlexW2062541888

What OpenQuestion holds

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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.