Evidence map›Paper›PMID 32725721›Full record

ArticlePharmacology research & perspectives2020

Ascorbate sensitizes human osteosarcoma cells to the cytostatic effects of cisplatin.

Naohiro Oka, Akiyoshi Komuro, Hisayuki Amano, Suman Dash, Masahiko Honda, Kazushige Ota, Shunji Nishimura, Takeshi Ueda, Masao Akagi, Hitoshi Okada

Open access · goldAbstract read
In one paragraph

Article in Pharmacology research & perspectives, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 14 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 2 institutions in 1 country.

Naohiro OkaDepartment of Orthopedics, Faculty of Medicine, Kindai University, Osaka, Japan.
Akiyoshi KomuroDepartment of Biochemistry, Faculty of Medicine, Kindai University, Osaka, Japan.
Hisayuki AmanoDepartment of Biochemistry, Faculty of Medicine, Kindai University, Osaka, Japan.
Suman DashGraduate School of Medical Sciences, Faculty of Medicine, Kindai University, Osaka, Japan.
Masahiko HondaDepartment of Biochemistry, Faculty of Medicine, Kindai University, Osaka, Japan.
Kazushige OtaDepartment of Biochemistry, Faculty of Medicine, Kindai University, Osaka, Japan.
Shunji NishimuraDepartment of Orthopedics, Faculty of Medicine, Kindai University, Osaka, Japan.
Takeshi UedaGraduate School of Medical Sciences, Faculty of Medicine, Kindai University, Osaka, Japan.
Masao AkagiDepartment of Orthopedics, Faculty of Medicine, Kindai University, Osaka, Japan.
Hitoshi OkadaGraduate School of Medical Sciences, Faculty of Medicine, Kindai University, Osaka, Japan.ORCID 0000-0001-5597-7212
Kindai University · JPKindai University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma (OS) is the most common malignant bone tumor and a leading cause of cancer-related deaths in children and adolescents. Current standard treatments for OS are a combination of preoperative chemotherapy, surgical resection, and adjuvant chemotherapy. Cisplatin is used as the standard chemotherapeutic for OS treatment, but it induces various adverse effects, limiting its clinical application. Improving treatment efficacy without increasing the cisplatin dosage is desirable. In the present study, we assessed the combined effect of ascorbate on cisplatin treatment using cultured human OS cells. Co-treatment with ascorbate induced greater suppression of OS cell but not nonmalignant cell proliferation. The chemosensitizing effect of ascorbate on cisplatin treatment was tightly linked to ROS production. Altered cellular redox state due to increased ROS production modified glycolysis and mitochondrial function in OS cells. In addition, OS cell sphere formation was markedly decreased, suggesting that ascorbate increased the treatment efficacy of cisplatin against stem-like cells in the cancer cell population. We also found that enhanced MYC signaling, ribosomal biogenesis, glycolysis, and mitochondrial respiration are key signatures in OS cells with cisplatin resistance. Furthermore, cisplatin resistance was reversed by ascorbate. Taken together, our findings provide a rationale for combining cisplatin with ascorbate in therapeutic strategies against OS.

Indexed as

Antineoplastic AgentsAscorbic AcidBone NeoplasmsCell Line, TumorCell ProliferationCisplatinDrug Resistance, NeoplasmHumansOsteosarcomaOxidation-ReductionAntineoplastic AgentsAscorbic AcidCisplatinchemoresistancemetabolismmitochondriaosteosarcomaROS

Identifiers

PMID32725721
PMCPMC7387887
OpenAlexW3045721620

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.