Evidence map›Paper›PMID 32181355›Full record

ArticleScience advances2020

MTH1 inhibitor amplifies the lethality of reactive oxygen species to tumor in photodynamic therapy.

Lingzhi Zhao, Junyao Li, Yaoquan Su, Liqiang Yang, Liu Chen, Lei Qiang, Yajing Wang, Huijing Xiang, Huijun Phoebe Tham, Juanjuan Peng and 1 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

24 citing papers in PubMed, 95 citations in OpenAlex.

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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

11 authors at 2 institutions in 2 countries.

Lingzhi ZhaoState Key Laboratory of Natural Medicine, The School of Basic Medical Sciences and Clinical Pharmacy, China Pharmaceutical University, Nanjing, Jiangsu 211198, China.ORCID 0000-0002-3944-9716
Junyao LiState Key Laboratory of Natural Medicine, The School of Basic Medical Sciences and Clinical Pharmacy, China Pharmaceutical University, Nanjing, Jiangsu 211198, China.ORCID 0000-0002-4160-9424
Yaoquan SuState Key Laboratory of Natural Medicine, The School of Basic Medical Sciences and Clinical Pharmacy, China Pharmaceutical University, Nanjing, Jiangsu 211198, China.ORCID 0000-0002-2605-5021
Liqiang YangState Key Laboratory of Natural Medicine, The School of Basic Medical Sciences and Clinical Pharmacy, China Pharmaceutical University, Nanjing, Jiangsu 211198, China.ORCID 0000-0001-7893-6691
Liu ChenState Key Laboratory of Natural Medicine, The School of Basic Medical Sciences and Clinical Pharmacy, China Pharmaceutical University, Nanjing, Jiangsu 211198, China.ORCID 0000-0002-4875-9257
Lei QiangState Key Laboratory of Natural Medicine, The School of Basic Medical Sciences and Clinical Pharmacy, China Pharmaceutical University, Nanjing, Jiangsu 211198, China.ORCID 0000-0002-7164-3164
Yajing WangState Key Laboratory of Natural Medicine, The School of Basic Medical Sciences and Clinical Pharmacy, China Pharmaceutical University, Nanjing, Jiangsu 211198, China.
Huijing XiangDivision of Chemistry and Biological Chemistry, School of Physical and Mathematical Sciences, Nanyang Technological University, 21 Nanyang Link, Singapore 637371, Singapore.
Huijun Phoebe ThamDivision of Chemistry and Biological Chemistry, School of Physical and Mathematical Sciences, Nanyang Technological University, 21 Nanyang Link, Singapore 637371, Singapore.
Juanjuan PengState Key Laboratory of Natural Medicine, The School of Basic Medical Sciences and Clinical Pharmacy, China Pharmaceutical University, Nanjing, Jiangsu 211198, China.ORCID 0000-0002-7114-7494
Yanli ZhaoDivision of Chemistry and Biological Chemistry, School of Physical and Mathematical Sciences, Nanyang Technological University, 21 Nanyang Link, Singapore 637371, Singapore.ORCID 0000-0002-9231-8360
China Pharmaceutical University · CNNanyang Technological University · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although photodynamic therapy (PDT) has been clinically applied tumor hypoxia still greatly restricts the performance of this oxygen-dependent oncological treatment. The delivery of oxygen donors to tumor may produce excessive reactive oxygen species (ROS) and damage the peripheral tissues. Herein, we developed a strategy to solve the hypoxia issue by enhancing the lethality of ROS. Before PDT, the ROS-defensing system of the cancer cells was obstructed by an inhibitor to MTH1, which is a key for the remediation of ROS-caused DNA damage. As a result, both nuclei and mitochondrial DNA damages were increased, remarkably promoting cellular apoptosis. The therapeutic results demonstrated that the performance of PDT can be improved by the MTH1 inhibitor, leading to efficient cancer cell killing effect in the hypoxic tumor. This strategy makes better use of the limited oxygen, holding the promise to achieve satisfactory therapeutic effect by PDT without generating redundant cytotoxic ROS.

Indexed as

AnimalsAntineoplastic AgentsApoptosisChlorophyllidesDNA, NeoplasmDNA RepairDNA Repair EnzymesDrug CarriersDrug CompoundingEnzyme InhibitorsFemaleGene ExpressionHCT116 CellsHeLa CellsHumansLight8-oxodGTPaseAntineoplastic AgentsChlorophyllidesDNA, NeoplasmDNA Repair EnzymesDrug CarriersEnzyme InhibitorsPhosphoric Monoester HydrolasesPhotosensitizing AgentsphytochlorinPorphyrinsPyrimidinesReactive Oxygen SpeciesTH588 compound

Identifiers

PMID32181355
PMCPMC7056313
OpenAlexW3009967958

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.