Evidence map›Paper›PMID 28598976›Full record

ArticlePloS one2017

The dynamic role of autophagy and MAPK signaling in determining cell fate under cisplatin stress in osteosarcoma cells.

Sudeshna Mukherjee, Subhra Dash, K Lohitesh, Rajdeep Chowdhury

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. 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
2.6field-weighted citation impact, top 10% 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, 31 citations in OpenAlex.

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  13. Article
  14. Role of autophagy in osteosarcoma.Journal of bone oncology · 2019
    Review
  15. Article
  16. Article
  17. Article
  18. OncoTargets and therapy · 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

4 authors at 1 institution in 1 country.

Sudeshna MukherjeeDepartment of Biological Sciences, Birla Institute of Technology and Science (BITS), Pilani, Rajasthan, India.
Subhra DashDepartment of Biological Sciences, Birla Institute of Technology and Science (BITS), Pilani, Rajasthan, India.
K LohiteshDepartment of Biological Sciences, Birla Institute of Technology and Science (BITS), Pilani, Rajasthan, India.
Rajdeep ChowdhuryDepartment of Biological Sciences, Birla Institute of Technology and Science (BITS), Pilani, Rajasthan, India.ORCID http://orcid.org/0000-0002-6041-0613
Birla Institute of Technology and Science, Pilani · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma (OS) is an aggressive bone malignancy commonly observed in children and adolescents. Sub-optimal therapy for years has irretrievably compromised the chances of OS patient survival; also, lack of extensive research on this rare disease has hindered therapeutic development. Cisplatin, a common anti-tumor drug, is currently an integral part of treatment regime for OS along with methotrexate and doxorubicin. However, toxicity issues associated with combination module impede OS therapy. Also, despite the proven benefits of cisplatin, acquisition of resistance remains a concern with cisplatin-based therapy. This prompted us to investigate the molecular effects of cisplatin exposure and changes associated with acquired resistance in OS cells. Cisplatin shock was found to activate MAPK signaling and autophagy in OS cells. An activation of JNK and autophagy acted as pro-survival strategy, while ERK1/2 triggered apoptotic signals upon cisplatin stress. A crosstalk between JNK and autophagy was observed. Maximal sensitivity to cisplatin was obtained with simultaneous inhibition of both autophagy and JNK pathway. Cisplatin resistant cells were further developed by repetitive drug exposure followed by clonal selection. The resistant cells showed an altered signaling circuitry upon cisplatin exposure. Our results provide valuable cues to possible molecular alterations that can be considered for development of improved therapeutic strategy against osteosarcoma.

Indexed as

Antineoplastic AgentsApoptosisAutophagyBone NeoplasmsCaspasesCell Line, TumorCell ProliferationCell SurvivalCisplatinDrug Resistance, NeoplasmHumansMAP Kinase Signaling SystemOsteosarcomaPhosphorylationTumor Suppressor Protein p53Antineoplastic AgentsCaspasesCisplatinTumor Suppressor Protein p53

Identifiers

PMID28598976
PMCPMC5466322
OpenAlexW2623719044

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.