Evidence map›Paper›PMID 34975339›Full record

ArticleInternational journal of biological sciences2022

Enhanced Intracellular Reactive Oxygen Species by Photodynamic Therapy Effectively Promotes Chemoresistant Cell Death.

Xiaolin Xu, Chenglong Wang, Peipei Zhang, Xuzhu Gao, Wencai Guan, Fanchen Wang, Xin Li, Jia Yuan, Hongjing Dou, Guoxiong Xu

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 25 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

10 authors at 3 institutions in 1 country.

Xiaolin XuResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai 201508, China.
Chenglong WangResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai 201508, China.
Peipei ZhangState Key Laboratory of Metal Matrix Composites, School of Materials Science and Engineering, Shanghai Jiao Tong University, Shanghai 200240, P. R. China.
Xuzhu GaoResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai 201508, China.
Wencai GuanResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai 201508, China.
Fanchen WangResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai 201508, China.
Xin LiResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai 201508, China.
Jia YuanResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai 201508, China.
Hongjing DouState Key Laboratory of Metal Matrix Composites, School of Materials Science and Engineering, Shanghai Jiao Tong University, Shanghai 200240, P. R. China.
Guoxiong XuResearch Center for Clinical Medicine, Jinshan Hospital, Fudan University, Shanghai 201508, China.
Jinshan Hospital of Fudan University · CNShanghai Medical College of Fudan University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-cancer chemo-drugs can cause a rapid elevation of intracellular reactive oxygen species (ROS) levels. An imbalance in ROS production and elimination systems leads to cancer cell resistance to chemotherapy. This study aimed to evaluate the mechanism and effect of ROS on multidrug resistance in various human chemoresistant cancer cells by detecting the changes in the amount of ROS, the expression of ROS-related and glycolysis-related genes, and cell death. We found that ROS was decreased while oxidative phosphorylation was increased in chemoresistant cells. We verified that the chemoresistance of cancer cells was achieved in two ways. First, chemoresistant cells preferred oxidative phosphorylation instead of anaerobic glycolysis for energy generation, which increased ATPase activity and produced much more ATP to provide energy. Second, ROS-scavenging systems were enhanced in chemoresistant cancer cells, which in turn decreased ROS amount and thus inhibited chemo-induced cell death. Our

Indexed as

Cell DeathOxidative PhosphorylationAnimalsCell Line, TumorDrug Resistance, NeoplasmFemaleGlycolysisHumansMiceMice, Inbred BALB CPhotochemotherapyReactive Oxygen SpeciesXenograft Model Antitumor AssaysReactive Oxygen SpeciesChemoresistanceglycolysismalignant tumoroxidative phosphorylationphotodynamic therapyROS

Identifiers

PMID34975339
PMCPMC8692137
OpenAlexW4200217473

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.