Evidence map›Paper›PMID 32397535›Full record

ReviewInternational journal of molecular sciences2020

Mitochondria Targeting as an Effective Strategy for Cancer Therapy.

Poorva Ghosh, Chantal Vidal, Sanchareeka Dey, Li Zhang

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed, 1 pooled it
10.5field-weighted citation impact, top 1% 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

142 citing papers in PubMed, 1 synthesis or guideline pooled it, 253 citations in OpenAlex.

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82 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Poorva GhoshDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.ORCID 0000-0001-6205-7078
Chantal VidalDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Sanchareeka DeyDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Li ZhangDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.ORCID 0000-0001-9242-0763
The University of Texas at Dallas · US

Funding

Cancer Prevention and Research Institute of Texas RP160617 & RP200021
6 · The paper itself

Abstract

Mitochondria are well known for their role in ATP production and biosynthesis of macromolecules. Importantly, increasing experimental evidence points to the roles of mitochondrial bioenergetics, dynamics, and signaling in tumorigenesis. Recent studies have shown that many types of cancer cells, including metastatic tumor cells, therapy-resistant tumor cells, and cancer stem cells, are reliant on mitochondrial respiration, and upregulate oxidative phosphorylation (OXPHOS) activity to fuel tumorigenesis. Mitochondrial metabolism is crucial for tumor proliferation, tumor survival, and metastasis. Mitochondrial OXPHOS dependency of cancer has been shown to underlie the development of resistance to chemotherapy and radiotherapy. Furthermore, recent studies have demonstrated that elevated heme synthesis and uptake leads to intensified mitochondrial respiration and ATP generation, thereby promoting tumorigenic functions in non-small cell lung cancer (NSCLC) cells. Also, lowering heme uptake/synthesis inhibits mitochondrial OXPHOS and effectively reduces oxygen consumption, thereby inhibiting cancer cell proliferation, migration, and tumor growth in NSCLC. Besides metabolic changes, mitochondrial dynamics such as fission and fusion are also altered in cancer cells. These alterations render mitochondria a vulnerable target for cancer therapy. This review summarizes recent advances in the understanding of mitochondrial alterations in cancer cells that contribute to tumorigenesis and the development of drug resistance. It highlights novel approaches involving mitochondria targeting in cancer therapy.

Indexed as

Molecular Targeted TherapyAntimetabolites, AntineoplasticCitric Acid CycleDrug Resistance, NeoplasmDynaminsEnergy MetabolismGlutamineGlycolysisGTP PhosphohydrolasesHemeHumansMitochondriaMitochondrial DynamicsMitochondrial ProteinsNeoplasm ProteinsNeoplasmsAntimetabolites, AntineoplasticDNM1L protein, humanDynaminsGlutamineGTP PhosphohydrolasesHemeMFN2 protein, humanMitochondrial ProteinsNeoplasm ProteinshememetabolismmitochondriaOXPHOS

Identifiers

PMID32397535
PMCPMC7247703
OpenAlexW3023426209

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.