Evidence map›Paper›PMID 31197132›Full record

ArticleCell death & disease2019

Vimentin activation in early apoptotic cancer cells errands survival pathways during DNA damage inducer CPT treatment in colon carcinoma model.

Souneek Chakraborty, Aviral Kumar, Mir Mohd Faheem, Archana Katoch, Anmol Kumar, Vijay Lakshmi Jamwal, Debasis Nayak, Aparna Golani, Reyaz Ur Rasool, Syed Mudabir Ahmad and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 47 citations in OpenAlex.

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  14. MicroRNAs as Modulators of Oral Tumorigenesis-A Focused Review.International journal of molecular sciences · 2021
    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

15 authors at 3 institutions in 1 country.

Souneek ChakrabortyAcademy of Scientific & Innovative Research (AcSIR), CSIR-Indian Institute of Integrative Medicine, Jammu, 180001, India.
Aviral KumarCancer Biology, CSIR-Centre for Cellular & Molecular Biology, Hyderabad, 500007, India.
Mir Mohd FaheemCancer Pharmacology Division, CSIR-Indian Institute of Integrative Medicine, Jammu, 180001, India.
Archana KatochAcademy of Scientific & Innovative Research (AcSIR), CSIR-Indian Institute of Integrative Medicine, Jammu, 180001, India.
Anmol KumarCancer Biology, CSIR-Centre for Cellular & Molecular Biology, Hyderabad, 500007, India.
Vijay Lakshmi JamwalPlant Biotechnology Division, CSIR-Indian Institute of Integrative Medicine, Jammu, 180001, India.
Debasis NayakAcademy of Scientific & Innovative Research (AcSIR), CSIR-Indian Institute of Integrative Medicine, Jammu, 180001, India.
Aparna GolaniCancer Biology, CSIR-Centre for Cellular & Molecular Biology, Hyderabad, 500007, India.
Reyaz Ur RasoolAcademy of Scientific & Innovative Research (AcSIR), CSIR-Indian Institute of Integrative Medicine, Jammu, 180001, India.
Syed Mudabir AhmadAcademy of Scientific & Innovative Research (AcSIR), CSIR-Indian Institute of Integrative Medicine, Jammu, 180001, India.
Jedy JoseCancer Biology, CSIR-Centre for Cellular & Molecular Biology, Hyderabad, 500007, India.
Rakesh KumarSchool of Biotechnology, Shri Mata Vaishno Devi University, Katra, 182320, India.ORCID http://orcid.org/0000-0002-0741-3663
Sumit G GandhiPlant Biotechnology Division, CSIR-Indian Institute of Integrative Medicine, Jammu, 180001, India.
Lekha Dinesh KumarCancer Biology, CSIR-Centre for Cellular & Molecular Biology, Hyderabad, 500007, India. lekha@ccmb.res.in.
Anindya GoswamiAcademy of Scientific & Innovative Research (AcSIR), CSIR-Indian Institute of Integrative Medicine, Jammu, 180001, India. agoswami@iiim.ac.in.
Indian Institute of Integrative Medicine · INCentre for Cellular and Molecular Biology · INShri Mata Vaishno Devi University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial to mesenchymal transitions (EMT) is a preparatory process for cancer cells to attain motility and further metastasis to distant sites. Majority of DNA damaging drugs have shown to develop EMT as one of the major mechanisms to attain drug resistance. Here we sought to understand the resistance/survival instincts of cancer cells during initial phase of drug treatment. We provide a tangible evidence of stimulation of EMT factors in Apc knockout colorectal carcinoma model. Our results implied that CPT-treated Apc knockout cohorts depicted increased pro-invasive and pro-survival factors (Vimentin/p

Indexed as

ApoptosisDNA DamageEpithelial-Mesenchymal TransitionAdenomatous Polyposis Coli ProteinAnimalsAtaxia Telangiectasia Mutated ProteinsCamptothecinCell Line, TumorCell ProliferationCell SurvivalColorectal NeoplasmsGene Expression Regulation, NeoplasticHumansMiceMice, KnockoutNF-kappa BAdenomatous Polyposis Coli ProteinAPC protein, humanAtaxia Telangiectasia Mutated ProteinsCamptothecinNF-kappa BVimentin

Identifiers

PMID31197132
PMCPMC6565729
OpenAlexW2952842834

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.