Evidence map›Paper›PMID 31615473›Full record

ArticleBMC cancer2019

Overexpression of iASPP is required for autophagy in response to oxidative stress in choriocarcinoma.

Ka-Kui Chan, Esther Shuk-Ying Wong, Ivy Tsz-Lo Wong, Claire Ling-Yang Cheung, Oscar Gee-Wan Wong, Hextan Yuen-Sheung Ngan, Annie Nga-Yin Cheung

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 20% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Molecular Basis of Hydatidiform Moles-A Systematic Review.International journal of molecular sciences · 2024
    Pooled it
  2. Article
  3. Article
  4. Article
  5. iASPP suppresses Gp78-mediated TMCO1 degradation to maintain CaProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  6. 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

7 authors at 1 institution in 2 countries.

Ka-Kui ChanDepartment of Pathology, Queen Mary Hospital, University of Hong Kong, Hong Kong SAR, China. kuiasdf@pathology.hku.hk.ORCID http://orcid.org/0000-0003-1498-8382
Esther Shuk-Ying WongDepartment of Pathology, Queen Mary Hospital, University of Hong Kong, Hong Kong SAR, China.
Ivy Tsz-Lo WongDepartment of Pathology, Queen Mary Hospital, University of Hong Kong, Hong Kong SAR, China.
Claire Ling-Yang CheungDepartment of Pathology, Queen Mary Hospital, University of Hong Kong, Hong Kong SAR, China.
Oscar Gee-Wan WongDepartment of Pathology, Queen Mary Hospital, University of Hong Kong, Hong Kong SAR, China.
Hextan Yuen-Sheung NganDepartment of Obstetrics and Gynaecology, Queen Mary Hospital, University of Hong Kong, Hong Kong SAR, China.
Annie Nga-Yin CheungDepartment of Pathology, Queen Mary Hospital, University of Hong Kong, Hong Kong SAR, China. anycheun@pathology.hku.hk.
Queen Mary Hospital · CN

Funding

Health and Medical Research Fund 01121336
6 · The paper itself

Abstract

backgroundGestational trophoblastic disease (GTD) is a heterogeneous group of diseases developed from trophoblasts. ASPP (Ankyrin-repeat, SH3-domain and proline-rich region containing protein) family proteins, ASPP1 and ASPP2, have been reported to be dysregulated in GTD. They modulate p53 activities and are responsible for multiple cellular processes. Nevertheless, the functional role of the ASPP family inhibitory member, iASPP, is not well characterized in GTD.

methodsTo study the functional role of iASPP in GTD, trophoblastic tissues from normal placentas, hydatidiform mole (HM) and choriocarcinoma were used for immunohistochemistry, whereas siRNAs were used to manipulate iASPP expression in choriocarcinoma cell lines and study the subsequent molecular changes.

resultsWe demonstrated that iASPP was overexpressed in both HM and choriocarcinoma when compared to normal placenta. Progressive increase in iASPP expression from HM to choriocarcinoma suggests that iASPP may be related to the development of trophoblastic malignancy. High iASPP expression in HM was also significantly associated with a high expression of autophagy-related protein LC3. Interestingly, iASPP silencing retarded the growth of choriocarcinoma through senescence instead of induction of apoptosis. LC3 expression decreased once iASPP was knocked down, suggesting a downregulation on autophagy. This may be due to iASPP downregulation rendered decrease in Atg5 expression and concomitantly hindered autophagy in choriocarcinoma cells. Autophagy inhibition per se had no effect on the growth of choriocarcinoma cells but increased the susceptibility of choriocarcinoma cells to oxidative stress, implying a protective role of iASPP against oxidative stress through autophagy in choriocarcinoma.

conclusionsiASPP regulates growth and the cellular responses towards oxidative stress in choriocarcinoma cells. Its overexpression is advantageous to the pathogenesis of GTD. (266 words).

Indexed as

AutophagyOxidative StressAdolescentAdultAutophagy-Related Protein 5Cell Line, TumorChoriocarcinomaFemaleFollow-Up StudiesGene Knockdown TechniquesHumansHydatidiform MoleIntracellular Signaling Peptides and ProteinsMicrotubule-Associated ProteinsMiddle AgedPlacentaATG5 protein, humanAutophagy-Related Protein 5Intracellular Signaling Peptides and ProteinsMAP1LC3A protein, humanMicrotubule-Associated ProteinsPPP1R13L protein, humanRepressor ProteinsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID31615473
PMCPMC6792270
OpenAlexW2980415452

What OpenQuestion holds

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LicenceCC BY
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.