Evidence map›Paper›PMID 33576438›Full record

ArticleMolecular medicine reports2021

Effect of mtDNA depletion from C6 glioma cells and characteristics of the generated C6ρ0 cells.

Youcai Jin, Guangxiang Luan, Ji Li, Honglun Wang, Zhenhua Wang, Bo Bai

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. 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 3 institutions in 1 country.

Youcai JinKey Laboratory of Tibetan Medicine Research, Northwest Institute of Plateau Biology, Chinese Academy of Sciences, Xining, Qinghai 810008, P.R. China.
Guangxiang LuanKey Laboratory of Tibetan Medicine Research, Northwest Institute of Plateau Biology, Chinese Academy of Sciences, Xining, Qinghai 810008, P.R. China.
Ji LiCenter for Mitochondria and Healthy Aging, College of Life Sciences, Yantai University, Yantai, Shandong 264005, P.R. China.
Honglun WangKey Laboratory of Tibetan Medicine Research, Northwest Institute of Plateau Biology, Chinese Academy of Sciences, Xining, Qinghai 810008, P.R. China.
Zhenhua WangCenter for Mitochondria and Healthy Aging, College of Life Sciences, Yantai University, Yantai, Shandong 264005, P.R. China.
Bo BaiKey Laboratory of Tibetan Medicine Research, Northwest Institute of Plateau Biology, Chinese Academy of Sciences, Xining, Qinghai 810008, P.R. China.
Institute of Tibetan Plateau Research · CNYantai University · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant tumors of the central nervous system (CNS) are among the types of cancer with the poorest prognosis and glioma is the commonest primary CNS tumor. A mitochondrial DNA (mtDNA)‑depleted cell line C6ρ0 was generated from C6 glioma cells after long‑term exposure to ethidium bromide and 2',3'‑dideoxycytidine in order to determine the effect of mtDNA damage on cell proliferation and pathological changes in glioma cells. Single cell clones were isolated and identified after 42 days of incubation. Repopulated cybrids were formed when the clonal C6ρ0 cells were fused with rat platelets and no difference was observed in their growth in a selective medium without uridine and pyruvate compared with the growth of the parent C6 cells. Disruption of mtDNA resulted in changes in mitochondrial morphology, decreased cell proliferation, reduced intracellular reactive oxygen species and intracellular ATP, along with decreased mtDNA and mitochondrial membrane potential in C6ρ0 cells compared with the C6 cells. Taken together, C6ρ0 cells without mtDNA were established for the first time and their characteristics were compared with parent cells. This C6ρ0 cell line could be used to explore the contribution of mitochondrial dysfunction and mtDNA mutations in the pathogenesis of glioma.

Indexed as

Adenosine TriphosphateAnimalsBrain NeoplasmsCell Line, TumorCell ProliferationDNA, MitochondrialGliomaIntracellular SpaceMembrane Potential, MitochondrialMitochondriaRatsReactive Oxygen SpeciesAdenosine TriphosphateDNA, MitochondrialReactive Oxygen SpeciesC6 gliomacytoplasmic hybridsmitochondrial DNAρ0

Identifiers

PMID33576438
PMCPMC7893707
OpenAlexW3127532425

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.