Evidence map›Paper›PMID 25300428›Full record

ArticleScientific reports2014

mtDNA germ line variation mediated ROS generates retrograde signaling and induces pro-cancerous metabolic features.

Rajnish Kumar Singh, Archita Srivastava, Ponnusamy Kalaiarasan, Siddharth Manvati, Rupali Chopra, Rameshwar N K Bamezai

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

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  5. Intimate Relations-Mitochondria and Ageing.International journal of molecular sciences · 2020
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  9. Article
  10. Article
  11. Article
  12. Review
  13. Mitochondrial genome instability in colorectal adenoma and adenocarcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    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.

Rajnish Kumar SinghNational Centre of Applied Human Genetics, School of life Sciences, Jawaharlal Nehru University, New Delhi, 110067, India.
Archita SrivastavaNational Centre of Applied Human Genetics, School of life Sciences, Jawaharlal Nehru University, New Delhi, 110067, India.
Ponnusamy KalaiarasanSchool of Biotechnology, Shri Mata Vaishno Devi University, Kakriyal, Katra, Jammu &Kashmir, 182320, India.
Siddharth ManvatiSchool of Biotechnology, Shri Mata Vaishno Devi University, Kakriyal, Katra, Jammu &Kashmir, 182320, India.
Rupali ChopraNational Centre of Applied Human Genetics, School of life Sciences, Jawaharlal Nehru University, New Delhi, 110067, India.
Rameshwar N K BamezaiNational Centre of Applied Human Genetics, School of life Sciences, Jawaharlal Nehru University, New Delhi, 110067, India.
Jawaharlal Nehru University · INShri Mata Vaishno Devi University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

mtDNA non-synonymous germ line variation (G10398A; p.A114T) has remained equivocal with least mechanistic understanding in showing an association with cancer. This has necessitated showing in-vitro how an over-expression within mitochondria of either of the variants produces higher intracellular ROS, resulting in differential anchorage dependent and independent growth. Both these features were observed to be relatively higher in ND3:114T variant. An elevated amount of intracellular carbonylated proteins and a reduced activity of a key glycolytic enzyme, Pyruvate kinase M2, along with high glucose uptake and lactate production were other pro-cancerous features observed. The retrograde signaling through surplus ROS was generated by post-ND3 over-expression regulated nuclear gene expression epigenetically, involving selectively the apoptotic-DDR-pathways. The feature of ND3 over-expression, inducing ROS mediated pro-cancerous features in the cells in in vitro, was replicated in a pilot study in a limited number of sporadic breast tumors, suggesting the importance of mitochondrial germ-line variant(s) in enabling the cells to acquire pro-cancerous features.

Indexed as

ApoptosisBreast NeoplasmsCell Transformation, NeoplasticDNA, MitochondrialFemaleGerm CellsHumansOxidative StressPyruvate KinaseReactive Oxygen SpeciesSignal TransductionDNA, MitochondrialPyruvate KinaseReactive Oxygen Species

Identifiers

PMID25300428
PMCPMC4192639
OpenAlexW2012788651

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.