Evidence map›Paper›PMID 28849075›Full record

ArticleMolecular medicine reports2017

Methylation of mitochondrial DNA displacement loop region regulates mitochondrial copy number in colorectal cancer.

Huan Tong, Linhao Zhang, Jinhang Gao, Shilei Wen, Hongying Zhou, Shi Feng

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

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  10. Mitochondrial epigenetic mechanisms in cancer: an updated overview.Frontiers in cell and developmental biology · 2025
    Review
  11. Article
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  14. Article
  15. Changes in Mitochondrial Epigenome in Type 2 Diabetes Mellitus.British journal of biomedical science · 2023
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Mitochondrial DNA Methylation and Human Diseases.International journal of molecular sciences · 2021
    Review
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 1 institution in 1 country.

Huan TongDepartment of Human Anatomy, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Linhao ZhangDepartment of Gastroenterology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Jinhang GaoDepartment of Gastroenterology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Shilei WenDepartment of Human Anatomy, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Hongying ZhouDepartment of Human Anatomy, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Shi FengDepartment of Human Anatomy, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is not established whether de‑methylation of the displacement loop (D‑loop) region if mitochondrial DNA (mtDNA) directly influences mtDNA copy number and further alters the cell cycle, apoptosis and cell proliferation in colorectal cancer. The current study employed cell viability assays, cell cycle analysis, and mtDNA methylation analysis using 5 colorectal cancer cell lines. The present results demonstrated that 5‑aza‑2'‑deoxycytidine (5‑AZA), a DNA hypomethylating agent, significantly increased proliferation of Lovo and Colo‑205 colorectal cancer cell lines. In Colo‑205 cells, the proportion of G0/G1 phase cells was increased following 5‑AZA treatment. Additionally, the apoptosis rate in Colo‑205 cells was decreased by 5‑AZA treatment. Compared with their controls, a significantly higher mtDNA copy number was observed in Colo‑205 and Lovo cells following 5‑AZA treatment. Notably, the Colo‑205 and Lovo cells had relatively higher methylation levels at the 4 and 6th/7th CpG sites of D‑loop region, respectively, compared with the levels at the corresponding sites following 5‑AZA treatment. However, in HCT116, SW480, LS‑174T, and HT‑29 cells, 5‑AZA treatment did not induce a significant change in proliferation, cell cycle, apoptosis and mtDNA copy number. Demethylation at the 4 and 6th/7th CpG sites of the D‑loop region of HCT116, SW480, LS‑174T and HT‑29 cells was not observed following 5‑AZA treatment. In conclusion, de‑methylation of specific sites on CpG islands of D‑loop promoter may lead to the elevation of mtDNA copy number in colorectal cancer, triggering alterations in biological behaviors, including increased cell proliferation, reduced apoptosis and a relative cell cycle arrest in G0/G1 phase.

Indexed as

DNA Copy Number VariationsDNA MethylationDNA, MitochondrialRegulatory Sequences, Nucleic AcidApoptosisAzacitidineBase SequenceCell CycleCell Line, TumorCell ProliferationCell SurvivalColorectal NeoplasmsCpG IslandsDecitabineEpigenesis, GeneticHumansAzacitidineDecitabineDNA, Mitochondrial

Identifiers

PMID28849075
PMCPMC5647067
OpenAlexW2747405735

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.