Evidence map›Paper›PMID 28906490›Full record

ArticleCell death & disease2017

POPX2 phosphatase regulates apoptosis through the TAK1-IKK-NF-κB pathway.

Ting Weng, Cheng-Gee Koh

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  7. Small-molecule IKKβ activation modulator (IKAM) targets MAP3K1 and inhibits pancreatic tumor growth.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Protein phosphatases in TLR signaling.Cell communication and signaling : CCS · 2021
    Review
  9. Review
  10. Review
  11. Article
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  13. Article
  14. TBC1D25 Regulates Cardiac Remodeling Through TAK1 Signaling Pathway.International journal of biological sciences · 2020
    Article
  15. Circular RNATheranostics · 2020
    Observational
  16. Article
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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

2 authors at 1 institution in 1 country.

Ting WengSchool of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore.
Cheng-Gee KohSchool of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore.
Nanyang Technological University · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemoresistance is one of the leading causes that contributes to tumor relapse and poor patient outcome after several rounds of drug therapy. The causes of chemoresistance are multi-factorial. Ultimately, it is the balance of pro- and anti-apoptotic activities in the cells. We have previously reported links between POPX2 serine/threonine phosphatase with cell motility and invasiveness of breast cancer cells. Here, we show that POPX2 plays a role in the regulation of apoptosis. The effect of POPX2 on apoptosis centers on the inactivation of TGF-β activated kinase (TAK1). TAK1 is essential for several important biological functions including innate immunity, development and cell survival. We find that POPX2 interacts directly with TAK1 and is able to dephosphorylate TAK1. Cells with lower levels of POPX2 exhibit higher TAK1 activity in response to etoposide (VP-16) treatment. This subsequently leads to increased translocation of NF-κB from the cytosol to the nucleus. Consequently, NF-κB-mediated transcription of anti-apoptotic proteins is upregulated to promote cell survival. On the other hand, cells with higher levels of POPX2 are more vulnerable to apoptosis induced by etoposide. Our data demonstrate that POPX2 is a negative regulator of TAK1 signaling pathway and modulates apoptosis through the regulation of TAK1 activity. As inhibition of TAK1 has been proposed to reduce chemoresistance and increase sensitivity to chemotherapy in certain types of cancer, modulation of POPX2 levels may provide an additional avenue and consideration in fine-tuning therapeutic response.

Indexed as

ApoptosisSignal TransductionAnimalsCell Line, TumorCell SurvivalDNA DamageEtoposideGene Knockdown TechniquesHumansI-kappa B KinaseMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesModels, BiologicalNF-kappa BPhosphoprotein PhosphatasesPhosphorylationEtoposideI-kappa B KinaseMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesNF-kappa BPhosphoprotein PhosphatasesPPM1F protein, human

Identifiers

PMID28906490
PMCPMC5636987
OpenAlexW2755867270

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.