Evidence map›Paper›PMID 24472424›Full record

ArticleMolecular cytogenetics2014

Induction of polyploidy by nuclear fusion mechanism upon decreased expression of the nuclear envelope protein LAP2β in the human osteosarcoma cell line U2OS.

Shirley Oren Ben-Shoshan, Amos J Simon, Jasmine Jacob-Hirsch, Sigal Shaklai, Nurit Paz-Yaacov, Ninette Amariglio, Gideon Rechavi, Luba Trakhtenbrot

Open access · goldAbstract read
In one paragraph

Article in Molecular cytogenetics, 2014. 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
1.0field-weighted citation impact, top 24% 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, 12 citations in OpenAlex.

  1. Review
  2. Cell-cell fusion in cancer: The next cancer hallmark?The international journal of biochemistry & cell biology · 2024
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  4. Review
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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

8 authors at 2 institutions in 1 country.

Shirley Oren Ben-Shoshan *Sheba Cancer Research Center, Chaim Sheba Medical Center, 52621, Tel-Hashomer, Israel.
Amos J Simon *Sheba Cancer Research Center, Chaim Sheba Medical Center, 52621, Tel-Hashomer, Israel.
Jasmine Jacob-HirschSheba Cancer Research Center, Chaim Sheba Medical Center, 52621, Tel-Hashomer, Israel.
Sigal ShaklaiSheba Cancer Research Center, Chaim Sheba Medical Center, 52621, Tel-Hashomer, Israel.
Nurit Paz-YaacovSheba Cancer Research Center, Chaim Sheba Medical Center, 52621, Tel-Hashomer, Israel.
Ninette AmariglioSheba Cancer Research Center, Chaim Sheba Medical Center, 52621, Tel-Hashomer, Israel.
Gideon RechaviSheba Cancer Research Center, Chaim Sheba Medical Center, 52621, Tel-Hashomer, Israel.
Luba TrakhtenbrotSheba Cancer Research Center, Chaim Sheba Medical Center, 52621, Tel-Hashomer, Israel.
Sheba Medical Center · ILTel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPolyploidy has been recognized for many years as an important hallmark of cancer cells. Polyploid cells can arise through cell fusion, endoreplication and abortive cell cycle. The inner nuclear membrane protein LAP2β plays key roles in nuclear envelope breakdown and reassembly during mitosis, initiation of replication and transcriptional repression. Here we studied the function of LAP2β in the maintenance of cell ploidy state, a role which has not yet been assigned to this protein.

resultsBy knocking down the expression of LAP2β, using both viral and non-viral RNAi approaches in osteosarcoma derived U2OS cells, we detected enlarged nuclear size, nearly doubling of DNA content and chromosomal duplications, as analyzed by fluorescent in situ hybridization and spectral karyotyping methodologies. Spectral karyotyping analyses revealed that near-hexaploid karyotypes of LAP2β knocked down cells consisted of not only seven duplicated chromosomal markers, as could be anticipated by genome duplication mechanism, but also of four single chromosomal markers. Furthermore, spectral karyotyping analysis revealed that both of two near-triploid U2OS sub-clones contained the seven markers that were duplicated in LAP2β knocked down cells, whereas the four single chromosomal markers were detected only in one of them. Gene expression profiling of LAP2β knocked down cells revealed that up to a third of the genes exhibiting significant changes in their expression are involved in cancer progression.

conclusionsOur results suggest that nuclear fusion mechanism underlies the polyploidization induction upon LAP2β reduced expression. Our study implies on a novel role of LAP2β in the maintenance of cell ploidy status. LAP2β depleted U2OS cells can serve as a model to investigate polyploidy and aneuploidy formation by nuclear fusion mechanism and its involvement in cancerogenesis.

Identifiers

PMID24472424
PMCPMC3926685
OpenAlexW2156078257

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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.