Evidence map›Paper›PMID 31822650›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2019

The Na+/K+ ATPase Inhibitor Ouabain Attenuates Stemness and Chemoresistance of Osteosarcoma Cells.

Weixiong Guo, Bo Wei, Tingting Cheng, Xiaotao Xu, Feiling Ruan, Min Xiang

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

7 citing papers in PubMed, 10 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

6 authors at 1 institution in 1 country.

Weixiong GuoDepartment of Orthopedics, The Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China (mainland).
Bo WeiDepartment of Orthopedics, The Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China (mainland).
Tingting ChengDepartment of Cardiovascular, The Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China (mainland).
Xiaotao XuDepartment of Operation Room, The Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China (mainland).
Feiling RuanDepartment of Operation Room, The Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China (mainland).
Min XiangDepartment of Orthopedics, Third Affiliated Hospital of Guangdong Medical University, Zhanjiang, China (mainland).
Guangdong Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND The purpose of this study was to explore the effects of the Na+/K+ ATPase inhibitor ouabain in regulating osteosarcoma (OS) cell stemness. MATERIAL AND METHODS Western blot, qPCR, sphere-forming analysis, DNA methylation analysis, and Ca²⁺ concentration detection were performed to evaluate the stem-like traits of cells and ouabain-induced effects and related mechanisms on OS cell stemness. Cell viability assessment was performed to evaluate the effect of ouabain on OS cell chemosensitivity. RESULTS Ouabain reduced the ALDH1 activity, the expression of critical stemness regulators, sphere size and number, and migration, invasion, and adhesion ability, but had little effects on cell viability. Additionally, the intracellular Ca²⁺ concentration and methylation level of the critical stemness regulators were higher in OS cells than in spheres formed by OS cells. Mechanistic studies revealed that ouabain leads to DNA methylation of stemness markers through increasing intracellular Ca²⁺ concentration. Notably, inhibition of Ca²⁺ channel or DNA methylation rescued the inhibition of ouabain on OS cell stemness. Additionally, ouabain enhances cisplatin sensitivity of OS cells, which is involved in Ca²⁺ channel and DNA methylation. CONCLUSIONS This work provides a potential compound for treating OS patients, especially OS patients with chemoresistance.

Indexed as

AzacitidineBone NeoplasmsCell AdhesionCell Line, TumorCell MovementCell SurvivalDNA MethylationDrug Resistance, NeoplasmEnzyme InhibitorsHumansNeoplasm InvasivenessNeoplastic Stem CellsOsteosarcomaOuabainSodium-Potassium-Exchanging ATPaseAzacitidineEnzyme InhibitorsOuabainSodium-Potassium-Exchanging ATPase

Identifiers

PMID31822650
PMCPMC6918806
OpenAlexW2996222297

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.