Evidence map›Paper›PMID 33558461›Full record

ArticleCell death & disease2021

Molecular imaging of the kinetics of hyperactivated ERK1/2-mediated autophagy during acquirement of chemoresistance.

Aniketh Bishnu, Pratham Phadte, Ajit Dhadve, Asmita Sakpal, Bharat Rekhi, Pritha Ray

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
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  3. Review
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  5. Autophagy-mediated ID1 turnover dictates chemo-resistant fate in ovarian cancer stem cells.Journal of experimental & clinical cancer research : CR · 2024
    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

6 authors at 3 institutions in 1 country.

Aniketh BishnuImaging Cell Signalling & Therapeutics Lab, Advanced Centre for Treatment, Research and Education in Cancer, TMC, Navi Mumbai, 410210, India.
Pratham PhadteImaging Cell Signalling & Therapeutics Lab, Advanced Centre for Treatment, Research and Education in Cancer, TMC, Navi Mumbai, 410210, India.
Ajit DhadveImaging Cell Signalling & Therapeutics Lab, Advanced Centre for Treatment, Research and Education in Cancer, TMC, Navi Mumbai, 410210, India.
Asmita SakpalImaging Cell Signalling & Therapeutics Lab, Advanced Centre for Treatment, Research and Education in Cancer, TMC, Navi Mumbai, 410210, India.
Bharat RekhiDepartment of Pathology, Tata Memorial Hospital, Mumbai, 400012, India.ORCID http://orcid.org/0000-0002-3509-4794
Pritha RayImaging Cell Signalling & Therapeutics Lab, Advanced Centre for Treatment, Research and Education in Cancer, TMC, Navi Mumbai, 410210, India. pray@actrec.gov.in.
Homi Bhabha National Institute · INAdvanced Centre for Treatment, Research and Education in Cancer · INTata Memorial Hospital · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alterations in key kinases and signaling pathways can fine-tune autophagic flux to promote the development of chemoresistance. Despite empirical evidences of strong association between enhanced autophagic flux with acquired chemoresistance, it is still not understood whether an ongoing autophagic flux is required for both initiation, as well as maintenance of chemoresistance, or is sufficient for one of the either steps. Utilizing indigenously developed cisplatin-paclitaxel-resistant models of ovarian cancer cells, we report an intriguing oscillation in chemotherapy-induced autophagic flux across stages of resistance, which was found to be specifically elevated at the early stages or onset of chemoresistance. Conversely, the sensitive cells and cells at late stages of resistance showed stalled and reduced autophagic flux. This increased flux at early stages of resistance was found to be dictated by a hyperactive ERK1/2 signaling, which when inhibited either pharmacologically (U0126/Trametinib) or genetically, reduced p62 degradation, number of LC3

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic AgentsAutophagyAutophagy-Related ProteinsCell Line, TumorCisplatinEnzyme ActivationFemaleHumansKineticsMiceMice, NudeMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Ovarian NeoplasmsAntineoplastic AgentsAutophagy-Related ProteinsCisplatinMAPK1 protein, humanMAPK3 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Paclitaxel

Identifiers

PMID33558461
PMCPMC7870816
OpenAlexW3128140358

What OpenQuestion holds

Textmetadata
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.