Evidence map›Paper›PMID 26727575›Full record

ArticleOncogenesis2016

Mieap-regulated mitochondrial quality control is frequently inactivated in human colorectal cancer.

H Kamino, Y Nakamura, M Tsuneki, H Sano, Y Miyamoto, N Kitamura, M Futamura, Y Kanai, H Taniguchi, D Shida and 4 more

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Trial
  2. Article
  3. The emerging mechanisms and functions of microautophagy.Nature reviews. Molecular cell biology · 2023
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  6. Mitophagy: An Emergence of New Player in Alzheimer's Disease.Frontiers in molecular neuroscience · 2022
    Review
  7. Article
  8. Review
  9. American journal of cancer research · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. 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

14 authors at 2 institutions in 1 country.

H KaminoDivision of Cancer Biology, National Cancer Center Research Institute, Tokyo, Japan.
Y NakamuraDivision of Cancer Biology, National Cancer Center Research Institute, Tokyo, Japan.
M TsunekiDivision of Cancer Biology, National Cancer Center Research Institute, Tokyo, Japan.
H SanoDivision of Cancer Biology, National Cancer Center Research Institute, Tokyo, Japan.
Y MiyamotoDivision of Cancer Biology, National Cancer Center Research Institute, Tokyo, Japan.
N KitamuraDivision of Cancer Biology, National Cancer Center Research Institute, Tokyo, Japan.
M FutamuraDivision of Cancer Biology, National Cancer Center Research Institute, Tokyo, Japan.
Y KanaiDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
H TaniguchiDepartment of Pathology and Clinical Laboratories, National Cancer Center Hospital, Tokyo, Japan.
D ShidaDepartment of Colorectal Surgery, National Cancer Center Hospital, Tokyo, Japan.
Y KanemitsuDepartment of Colorectal Surgery, National Cancer Center Hospital, Tokyo, Japan.
Y MoriyaDepartment of Colorectal Surgery, National Cancer Center Hospital, Tokyo, Japan.
K YoshidaDepartment of Surgical Oncology, Gifu University Graduate School of Medicine, Gifu, Japan.
H ArakawaDivision of Cancer Biology, National Cancer Center Research Institute, Tokyo, Japan.
Tokyo National Hospital · JPGifu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mieap, a p53-inducible protein, controls mitochondrial quality by repairing or eliminating unhealthy mitochondria. BNIP3 and NIX are critical mediators for the Mieap-regulated mitochondrial quality control. Mieap suppresses murine intestinal tumor via its mitochondrial quality control function. To explore the role of the Mieap-regulated mitochondria quality control function in colorectal cancer patients, we examined the statuses of p53, Mieap, BNIP3 and NIX in 57 primary colorectal cancer tissues. Promoter methylation of the Mieap and BNIP3 genes was found in 9% and 47% of colorectal cancer cases, respectively, whereas p53 mutation was found in more than 50% of colorectal cancer tissues lacking methylation of the Mieap and BNIP3 promoters, implying that the p53/Mieap/BNIP3-regulated mitochondria quality control pathway is inactivated in more than 70% of colorectal cancer patients. In LS174T colorectal cancer cells, hypoxia activated the Mieap-regulated mitochondria quality control function. Knockdown of p53, Mieap or BNIP3 in LS174T cells severely impaired the hypoxia-activated function, leading to the accumulation of unhealthy mitochondria and increase of mitochondrial reactive oxygen species generation. The mitochondrial reactive oxygen species generated by unhealthy mitochondria in the p53/Mieap/BNIP3-deficient cells remarkably enhanced cancer cell migration and invasion under hypoxic condition. These results suggest that the Mieap-regulated mitochondria quality control has a critical role in colorectal cancer suppression in the in vivo hypoxic tumor microenvironment.

Identifiers

PMID26727575
PMCPMC4728673
OpenAlexW2231591590

What OpenQuestion holds

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LicenceCC BY
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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.