Evidence map›Paper›PMID 29211704›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2017

Histone Deacetylase (HDAC) Inhibitor, Suberoylanilide Hydroxamic Acid (SAHA), Induces Apoptosis in Prostate Cancer Cell Lines via the Akt/FOXO3a Signaling Pathway.

Xuan-Yan Shi, Wei Ding, Tie-Qiu Li, Yi-Xiong Zhang, Shan-Chao Zhao

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 60 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 3 institutions in 1 country.

Xuan-Yan ShiDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China (mainland).
Wei DingDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China (mainland).
Tie-Qiu LiDepartment of Urology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan normal University, Changsha, Hunan, China (mainland).
Yi-Xiong ZhangDepartment of Emergency, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan normal University, Changsha, Hunan, China (mainland).
Shan-Chao ZhaoDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China (mainland).
Hunan Provincial People's Hospital · CNSouthern Medical University · CNNanfang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Histone deacetylase (HDAC) inhibitors are emerging as a new class of anti-cancer drugs that promote cancer cell apoptosis, and include suberoylanilide hydroxamic acid (SAHA). The aim of this study was to investigate the mechanism of SAHA-induced apoptosis in human prostate cancer cell lines, DU145 and PC-3. MATERIAL AND METHODS Cell lines, DU145 and PC-3, were studied before and after treatment with SAHA. The effects of SAHA treatment on cell proliferation were studied using the MTT cell proliferation assay. Annexin-V-fluorescein isothiocyanate (FITC) and propidium iodide (PI) staining were used to study the effects of SAHA treatment on cell apoptosis. Western blotting, quantitative polymerase chain reaction (qPCR) and short interfering (si)RNA assays were performed to study the effects of SAHA treatment on apoptotic and cell cycle proteins and the Akt/FOXO3a signaling pathway. RESULTS Treatment with SAHA inhibited cell proliferation in human prostate cancer cell lines DU145 and PC-3 cells in a dose-dependent way. Cell cycle analysis and Annexin-V FITC/PI staining showed that treatment with SAHA resulted in G2/M cell cycle arrest and increased cell apoptosis in a dose-dependent way. Also, treatment with SAHA reduced the protein expression levels cyclin B and cyclin A2 and promoted the activation of FOXO3a by inhibiting Akt activation. Western blotting, the siRNA assay, and qPCR showed that FOXO3a, the Bcl-2 family of proteins, survivin, and FasL were involved in SAHA-induced apoptosis in prostate cancer cells grown in vitro. CONCLUSIONS Treatment with SAHA promoted apoptosis via the Akt/FOXO3a signaling pathway in prostate cancer cells in vitro.

Indexed as

Annexin A5Antineoplastic AgentsApoptosisCell CycleCell Line, TumorCell ProliferationCell SurvivalForkhead Box Protein O3Histone Deacetylase InhibitorsHistone DeacetylasesHumansHydroxamic AcidsInhibitor of Apoptosis ProteinsMaleProstatic NeoplasmsProto-Oncogene Proteins c-aktAnnexin A5Antineoplastic AgentsForkhead Box Protein O3FOXO3 protein, humanHistone Deacetylase InhibitorsHistone DeacetylasesHydroxamic AcidsInhibitor of Apoptosis ProteinsProto-Oncogene Proteins c-aktVorinostat

Identifiers

PMID29211704
PMCPMC5727751
OpenAlexW2773163641

What OpenQuestion holds

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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.