Evidence map›Paper›PMID 18597698›Full record

ArticleJournal of experimental & clinical cancer research : CR2008

CSE1L/CAS, the cellular apoptosis susceptibility protein, enhances invasion and metastasis but not proliferation of cancer cells.

Ching-Fong Liao, Shue-Fen Luo, Li-Tzu Li, Chuang-Yu Lin, Ying-Chun Chen, Ming-Chung Jiang

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2008. 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
1.8field-weighted citation impact, top 16% 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, 56 citations in OpenAlex.

  1. Article
  2. Role of CSE1L expression in determining recurrence and survival of laryngeal tumors.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2022
    Article
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  7. Roles of the CSE1L-mediated nuclear import pathway in epigenetic silencing.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  8. Article
  9. CAS (CSE1L) signaling pathway in tumor progression and its potential as a biomarker and target for targeted therapy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
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  11. Article
  12. Article
  13. CSE1L, DIDO1 and RBM39 in colorectal adenoma to carcinoma progression.Cellular oncology (Dordrecht, Netherlands) · 2012
    Article
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  15. 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

6 authors at 4 institutions in 1 country.

Ching-Fong LiaoInstitute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan, PR China. liao@gate.sinica.edu.tw
Shue-Fen Luo
Li-Tzu Li
Chuang-Yu Lin
Ying-Chun Chen
Ming-Chung Jiang
Academia Sinica · TWInstitute of Cellular and Organismic Biology, Academia Sinica · TWChang Gung University · TWTungs' Taichung MetroHarbor Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe cellular apoptosis susceptibility (CAS) protein is regarded as a proliferation-associated protein that associates with tumour proliferation as it associates with microtubule and functions in the mitotic spindle checkpoint. However, there is no any actual experimental study showing CAS (or CSE1 and CSE1L) can increase the proliferation of cancer cells. Previous pathological study has reported that CAS was strongly positive stained in all of the metastasis melanoma that be examined. Thus, CAS may regulate the invasion and metastasis of cancers. CAS is highly expressed in cancers; if CAS is associated with cancer proliferation, then increased CAS expression should be able to increase the proliferation of cancer cells. We studied whether increased CAS expression can increase cancer cell proliferation and whether CAS regulates the invasion of cancer cells.

methodsWe enhanced or reduced CAS expression by transfecting CAS or anti-CAS expression vectors into human MCF-7 breast cancer cells. The proliferations of cells were determined by trypan blue exclusion assay and flow cytometry analysis. Invasion of cancer cells were determined by matrigel-based invasion assay.

resultsOur studies showed that increased CAS expression was unable to enhance cancer cell proliferation. Immunofluorescence showed CAS was distributed in cytoplasm areas near cell membrane and cell protrusions. CAS was localized in cytoplasmic vesicle and immunogold electronmicroscopy showed CAS was located in vesicle membrane. CAS overexpression enhanced matrix metalloproteinase-2 (MMP-2) secretion and cancer cell invasion. Animal experiments showed CAS reduction inhibited the metastasis of B16-F10 melanoma cells by 56% in C57BL/6 mice.

conclusionOur results indicate that CAS increases the invasion but not the proliferation of cancer cells. Thus, CAS plus ECM-degradation proteinases may be used as the markers for predicting the advance of tumour metastasis.

Indexed as

Neoplasm InvasivenessNeoplasm MetastasisAnimalsBreast NeoplasmsCell Line, TumorCell ProliferationCellular Apoptosis Susceptibility ProteinFemaleFlow CytometryFluorescent Antibody TechniqueHumansImmunoblottingMiceMice, Inbred C57BLNeoplasmsCellular Apoptosis Susceptibility Protein

Identifiers

PMID18597698
PMCPMC2474842
OpenAlexW2104321192

What OpenQuestion holds

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Registered trials

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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.