Evidence map›Paper›PMID 17018150›Full record

ArticleBMC cancer2006

Targeting of mutant hogg1 in mammalian mitochondria and nucleus: effect on cellular survival upon oxidative stress.

Aditi Chatterjee, Elizabeth Mambo, Yonggang Zhang, Theodore Deweese, David Sidransky

Open access · goldAbstract readComparative Study
In one paragraph

Article in BMC cancer, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 13% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. The hOGG1 Ser326Cys polymorphism contributes to digestive system cancer susceptibility: evidence from 48 case-control studies.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Pooled it
  2. Biochemical analysis of HDNA repair · 2024
    Article
  3. Mitochondrial CaArteriosclerosis, thrombosis, and vascular biology · 2022
    Article
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  17. Mitochondria in lung biology and pathology: more than just a powerhouse.American journal of physiology. Lung cellular and molecular physiology · 2014
    Review
  18. Article
  19. Article
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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

5 authors at 2 institutions in 1 country.

Aditi ChatterjeeDepartment of Otolaryngology-Head and Neck Surgery, Head and Neck Cancer Research Division, 1550 Orleans Street, Johns Hopkins University School of Medicine, Cancer Research Building II, Room 5 06, Baltimore, MD 21231, USA. chattad@jhmi.edu
Elizabeth Mambo
Yonggang Zhang
Theodore Deweese
David Sidransky
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

INTEGRATED DEVELOPMENT OF NOVEL MOLECULAR MARKERSU01CA084986 · NCI · JOHNS HOPKINS UNIVERSITY · PI SIDRANSKY, DAVID · 1999 to 2014
$33.8M
NCI NIH HHS 1 U01 CA84986-06NCI NIH HHS U01 CA084986
6 · The paper itself

Abstract

backgroundOxidative damage to mitochondrial DNA has been implicated as a causative factor in a wide variety of degenerative diseases, aging and cancer. The modified guanine, 7,8-dihydro-8-oxoguanine (also known as 8-hydroxyguanine) is one of the major oxidized bases generated in DNA by reactive oxygen species and has gained most of the attention in recent years as a marker of oxidative DNA injury and its suspected role in the initiation of carcinogenesis. 8-hydroxyguanine is removed by hOgg1, a DNA glycosylase/AP lyase involved in the base excision repair pathway.

methodsWe over-expressed wild type and R229Q mutant hOGG1 in the nucleus and mitochondria of cells lacking mitochondrial hOGG1 expression through an expression vector containing nuclear and mitochondrial targeting sequence respectively. We used quantitative real time PCR to analyze mtDNA integrity after exposure to oxidative damaging agents, in cells transfected with or without mitochondrially-targeted mutant hogg1.

resultOver-expression of wild type hOgg1 in both nucleus and mitochondria resulted in increased cellular survival when compared to vector or mutant over-expression of hOGG1. Interestingly, mitochondrially-targeted mutant hogg1 resulted in more cell death than nuclear targeted mutant hogg1 upon exposure of cells to oxidative damage. Additional we examined mitochondrial DNA integrity after oxidative damage exposure using real-time quantitative PCR. The presence of mutant hogg1 in the mitochondria resulted in reduced mitochondrial DNA integrity when compared to the wild type. Our work indicates that the R229Q hOGG1 mutation failed to protect cells from oxidative damage and that such mutations in cancer may be more detrimental to cellular survival when present in the mitochondria than in the nucleus.

conclusionThese findings suggest that deficiencies in hOGG1, especially in the mitochondria may lead to reduced mitochondrial DNA integrity, consequently resulting in decreased cell viability.

Indexed as

MutationArginineAsparagineCell NucleusCell SurvivalDNA GlycosylasesDNA, MitochondrialDNA, NeoplasmGene TargetingHeLa CellsHumansMitochondriaOxidative StressArginineAsparagineDNA GlycosylasesDNA, MitochondrialDNA, Neoplasmoxoguanine glycosylase 1, human

Identifiers

PMID17018150
PMCPMC1633743
OpenAlexW1832212699

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.