Evidence map›Paper›PMID 28229963›Full record

ArticleJournal of biosciences2017

Constitutively activated ERK sensitizes cancer cells to doxorubicin: Involvement of p53-EGFR-ERK pathway.

Ratna Kumari, Surbhi Chouhan, Snahlata Singh, Rishi Raj Chhipa, Amrendra Kumar Ajay, Manoj Kumar Bhat

Abstract read
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In one paragraph

Article in Journal of biosciences, 2017. 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
1.0field-weighted citation impact, top 25% 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, 33 citations in OpenAlex.

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  16. ERK is a Pivotal Player of Chemo-Immune-Resistance in Cancer.International journal of molecular sciences · 2019
    Review
  17. Article
  18. Article
  19. Cancer cell international · 2018
    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

6 authors at 2 institutions in 1 country.

Ratna KumariNational Centre for Cell Science, Savitribai Phule Pune University Campus, Ganeshkhind, Pune 411 007, India.
Surbhi Chouhan
Snahlata Singh
Rishi Raj Chhipa
Amrendra Kumar Ajay
Manoj Kumar Bhat
National Centre for Cell Science · INSavitribai Phule Pune University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumour suppressor gene p53 is mutated in approximately 50% of the human cancers. p53 is involved in genotoxic stress-induced cellular responses. The role of EGFR and ERK in DNA-damage-induced apoptosis is well known. We investigated the involvement of activation of ERK signalling as a consequence of non-functional p53, in sensitivity of cells to doxorubicin. We performed cell survival assays in cancer cell lines with varying p53 status: MCF-7 (wild-type p53, WTp53), MDA MB-468 (mutant p53, MUTp53), H1299 (absence of p53, NULLp53) and an isogenic cell line MCF-7As (WTp53 abrogated). Our results indicate that enhanced chemosensitivity of cells lacking wild-type p53 function is because of elevated levels of EGFR which activates ERK. Additionally, we noted that independent of p53 status, pERK contributes to doxorubicin-induced cell death.

Indexed as

ApoptosisCell ProliferationCell SurvivalDNA DamageDoxorubicinDrug Resistance, NeoplasmErbB ReceptorsHumansMAP Kinase Signaling SystemMCF-7 CellsNeoplasmsTumor Suppressor Protein p53DoxorubicinEGFR protein, humanErbB ReceptorsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID28229963
OpenAlexW2585899330

What OpenQuestion holds

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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.