Evidence map›Paper›PMID 34134082›Full record

ArticleNeoplasia (New York, N.Y.)2021

Reduction in mitochondrial oxidative stress mediates hypoxia-induced resistance to cisplatin in human transitional cell carcinoma cells.

Myung-Chul Kim, Sung-Hyun Hwang, Yeseul Yang, Na-Yon Kim, Yongbaek Kim

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 32% 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

8 citing papers in PubMed, 12 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

5 authors at 1 institution in 2 countries.

Myung-Chul KimLaboratory of Clinical Pathology, College of Veterinary Medicine, Seoul National University, Seoul, The Republic of Korea; BK21 PLUS Program for Creative Veterinary Science Research, College of Veterinary Medicine, Seoul National University, Seoul, The Republic of Korea; Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FL, USA.
Sung-Hyun HwangLaboratory of Clinical Pathology, College of Veterinary Medicine, Seoul National University, Seoul, The Republic of Korea; BK21 PLUS Program for Creative Veterinary Science Research, College of Veterinary Medicine, Seoul National University, Seoul, The Republic of Korea.
Yeseul YangLaboratory of Clinical Pathology, College of Veterinary Medicine, Seoul National University, Seoul, The Republic of Korea; BK21 PLUS Program for Creative Veterinary Science Research, College of Veterinary Medicine, Seoul National University, Seoul, The Republic of Korea.
Na-Yon KimLaboratory of Clinical Pathology, College of Veterinary Medicine, Seoul National University, Seoul, The Republic of Korea; BK21 PLUS Program for Creative Veterinary Science Research, College of Veterinary Medicine, Seoul National University, Seoul, The Republic of Korea.
Yongbaek KimLaboratory of Clinical Pathology, College of Veterinary Medicine, Seoul National University, Seoul, The Republic of Korea; Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul, The Republic of Korea. Electronic address: yongbaek@snu.ac.kr.
Seoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor hypoxia is known to promote the acquisition of more aggressive phenotypes in human transitional cell carcinoma (TCC), including drug resistance. Accumulating evidence suggests that mitochondria play a central role in the chemoresistance of TCC. However, the role of mitochondria in the hypoxia-induced drug resistance in TCC remains elusive. The present study investigated the function of mitochondria in the drug resistance using a TCC cell line under hypoxic conditions. In vitro hypoxia (0.1% O

Indexed as

ApoptosisCarcinoma, Transitional CellCell Line, TumorCell SurvivalCisplatinDNA FragmentationDrug Resistance, NeoplasmHumansHypoxiaMembrane Potential, MitochondrialMitochondriaModels, BiologicalOxidative StressReactive Oxygen SpeciesTumor HypoxiaCisplatinReactive Oxygen SpeciesDrug resistanceHypoxiaMitochondriamtDNAOxidative stress

Identifiers

PMID34134082
PMCPMC8208898
OpenAlexW3166132470

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.