Evidence map›Paper›PMID 30953339›Full record

ArticleGenes & genomics2019

Reversine induces caspase-dependent apoptosis of human osteosarcoma cells through extrinsic and intrinsic apoptotic signaling pathways.

Jae-Sung Kim, In-A Cho, Kyeong-Rok Kang, HyangI Lim, Tae-Hyeon Kim, Sun-Kyoung Yu, Heung-Joong Kim, Seul Ah Lee, Sung Min Moon, Hong Sung Chun and 2 more

Abstract read
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In one paragraph

Article in Genes & genomics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  4. Arctigenin induces caspase-dependent apoptosis in FaDu human pharyngeal carcinoma cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022
    Article
  5. Deubiquitinating Enzyme USP12 Regulates the Pro-Apoptosis Protein Bax.International journal of molecular sciences · 2022
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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

12 authors at 1 institution in 1 country.

Jae-Sung KimInstitute of Dental Science, Chosun University, Gwangju, 61452, Republic of Korea.
In-A ChoInstitute of Dental Science, Chosun University, Gwangju, 61452, Republic of Korea.
Kyeong-Rok KangInstitute of Dental Science, Chosun University, Gwangju, 61452, Republic of Korea.
HyangI LimInstitute of Dental Science, Chosun University, Gwangju, 61452, Republic of Korea.
Tae-Hyeon KimInstitute of Dental Science, Chosun University, Gwangju, 61452, Republic of Korea.
Sun-Kyoung YuInstitute of Dental Science, Chosun University, Gwangju, 61452, Republic of Korea.
Heung-Joong KimInstitute of Dental Science, Chosun University, Gwangju, 61452, Republic of Korea.
Seul Ah LeeInstitute of Dental Science, Chosun University, Gwangju, 61452, Republic of Korea.
Sung Min MoonInstitute of Dental Science, Chosun University, Gwangju, 61452, Republic of Korea.
Hong Sung ChunDepartment of Biomedical Science, Chosun University, Gwangju, 61452, Republic of Korea.
Chun Sung KimInstitute of Dental Science, Chosun University, Gwangju, 61452, Republic of Korea.
Do Kyung KimInstitute of Dental Science, Chosun University, Gwangju, 61452, Republic of Korea. kdk@chosun.ac.kr.ORCID 0000-0001-6254-946X
Chosun University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe 2-(4-morpholinoanilino)-6-cyclohexylaminopurine (reversine) acts as a chemopreventive agent and induces apoptotic cell death in various cancer cells. However, the anticancer effects of reversine on osteosarcoma cells are not clearly established.

objectiveThe purpose of this study was to investigate the effect of reversine on cell proliferation and induction of apoptosis in human osteosarcoma cells.

methodsCell viability assay, histological analysis, DAPI staining, caspase activation analysis, flow cytometric analysis and immunoblotting were carried out in MG-63 osteosarcoma cells.

resultsReversine inhibited the growth of cells in a dose-dependent manner and induced nuclear condensation and fragmentation. Reversine-treated cells showed caspase-3/7 activation and increased apoptosis versus control cells. FasL, a death ligand associated with extrinsic apoptotic signaling pathways, was significantly up-regulated by reversine treatment. Moreover, the caspase-8, a part of the extrinsic apoptotic pathway, was activated by reversine treatments. Expressions of anti-apoptotic factors such as Bcl-2 and Bcl-xL, components of the mitochondria dependent intrinsic apoptosis pathway, significantly decreased following reversine treatment. The expressions of pro-apoptotic factors such as BAX, BAD and caspase-9 increased by reversine treatments. In addition, reversine activated caspase-3 and Poly (ADP-ribose) polymerase (PARP) to induce cell death. The Z-VAD-fmk significantly inhibited cell death through the suppression of caspase-3 expression in MG-63 cells treated with reversine.

conclusionThese results suggest that the reversine may inhibit cell proliferation and induce apoptotic cell death in MG-63 osteosarcoma cells through both the mitochondria-mediated intrinsic pathway and the death receptor-mediated extrinsic pathway, and may have potential properties for the discovery of anti-cancer agents.

Indexed as

Antineoplastic AgentsApoptosisCaspasesCell Line, TumorCell ProliferationHumansMorpholinesOsteosarcomaPurinesSignal Transduction2-(4-morpholinoanilino)-6-cyclohexylaminopurineAntineoplastic AgentsCaspasesMorpholinesPurinesAnticancer activityApoptosisCaspaseCell deathOsteosarcomaReversine

Identifiers

PMID30953339
OpenAlexW2930304824

What OpenQuestion holds

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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.