Evidence map›Paper›PMID 34533888›Full record

ReviewCancer science2021

Mitochondria: Endosymbiont bacteria DNA sequence as a target against cancer.

Hiroki Nagase, Takayoshi Watanabe, Nobuko Koshikawa, Seigi Yamamoto, Keizo Takenaga, Jason Lin

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 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
0.2field-weighted citation impact, top 47% 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. Review
  2. 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.

Hiroki NagaseDivision of Cancer Genetics, Chiba Cancer Center Research Institute, Chiba, Japan.ORCID https://orcid.org/0000-0002-3992-5399
Takayoshi WatanabeDivision of Innovative Cancer Therapeutics, Chiba Cancer Center Research Institute, Chiba, Japan.
Nobuko KoshikawaDivision of Cancer Genetics, Chiba Cancer Center Research Institute, Chiba, Japan.
Seigi YamamotoDivision of Cancer Genetics, Chiba Cancer Center Research Institute, Chiba, Japan.
Keizo TakenagaDivision of Cancer Genetics, Chiba Cancer Center Research Institute, Chiba, Japan.ORCID https://orcid.org/0000-0002-5341-6742
Jason LinDivision of Cancer Genetics, Chiba Cancer Center Research Institute, Chiba, Japan.ORCID https://orcid.org/0000-0002-8086-3185
Chiba Cancer Center · JP

Funding

Japan Agency for Medical Research and Development 18ae0101051Japan Agency for Medical Research and Development 21ek0109495Japan Agency for Medical Research and Development 21zf0127001Japan Society for the Promotion of Science 17H03602Japan Society for the Promotion of Science JP16H01579Japan Society for the Promotion of Science JP20H03540Japan Society for the Promotion of Science JP26290060the Princess Takamatsu Cancer Research FundThe Tokyo Biochemical Research Foundation
6 · The paper itself

Abstract

As the energy factory for the cell, the mitochondrion, through its role of adenosine triphosphate production by oxidative phosphorylation, can be regarded as the guardian of well regulated cellular metabolism; the integrity of mitochondrial functions, however, is particularly vulnerable in cancer due to the lack of superstructures such as histone and lamina folds to protect the mitochondrial genome from unintended exposure, which consequently elevates risks of mutation. In cancer, mechanisms responsible for enforcing quality control surveillance for identifying and eliminating defective mitochondria are often poorly regulated, and certain uneliminated mitochondrial DNA (mtDNA) mutations and polymorphisms can be advantageous for the proliferation, progression, and metastasis of tumor cells. Such pathogenic mtDNA aberrations are likely to increase and occasionally be homoplasmic in cancer cells and, intriguingly, in normal cells in the proximity of tumor microenvironments as well. Distinct characteristics of these abnormalities in mtDNA may provide a new path for cancer therapy. Here we discuss a promising novel therapeutic strategy, using the sequence-specific properties of pyrrole-imidazole polyamide-triphenylphosphonium conjugates, against cancer for clearing abnormal mtDNA by reactivating mitochondrial quality control surveillance.

Indexed as

Genome, MitochondrialHumansMitochondriaMolecular Targeted TherapyMutationNeoplasmsOrganophosphorus CompoundsOrganophosphorus Compoundsage-related disorderanticancer therapyapoptosisautophagyBcl familyexocytosismitochondriamitochondrial diseasemitochondrial quality controlmitophagymtDNAmutationpolymorphismpyrrole-imidazole polyamidereactive oxygen speciessenescencetriphenylphosphonium

Identifiers

PMID34533888
PMCPMC8645765
OpenAlexW3200656657

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.