Evidence map›Paper›PMID 30132513›Full record

ArticleInternational journal of oncology2018

Knockdown of anti-silencing function 1B histone chaperone induces cell apoptosis via repressing PI3K/Akt pathway in prostate cancer.

Guangye Han, Xinjun Zhang, Pei Liu, Quanfeng Yu, Zeyu Li, Qinnan Yu, Xiaoxia Wei

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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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

7 authors at 2 institutions in 1 country.

Guangye HanThe Second Ward of Urology Department, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China.
Xinjun ZhangThe First Ward of Urology Department, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China.
Pei LiuThe Second Ward of Urology Department, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China.
Quanfeng YuThe Second Ward of Urology Department, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China.
Zeyu LiThe Second Ward of Urology Department, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China.
Qinnan YuThe First Ward of Urology Department, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China.
Xiaoxia WeiThe Second Ward of Infection Department, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China.
First Affiliated Hospital of Xinxiang Medical University · CNXinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PCa) is one of the most common malignancies among males worldwide. Anti-silencing function 1B histone chaperone (ASF1B) has been reported to be involved in PCa. The present study aimed to investigate the role and molecular mechanism of ASF1B in PCa. Data of genes were obtained from The Cancer Genome Atlas database. The core gene was identified using the DAVID website. Cell viability and colony formation were detected using a cell counting kit-8 assay and crystal violet staining, respectively. Cell cycle distribution and apoptosis were assessed using flow cytometry analysis. The corresponding factors were analyzed by reverse transcription-quantitative polymerase chain reaction and western blotting. It was demonstrated that ASF1B was highly expressed in the PCa tissues and cells compared with the non-PCa tissues and cells, respectively. While siRNA-ASF1B significantly reduced the viability and colony formation, it promoted apoptosis, G1 phase cell cycle arrest of LNCap as well as C4-2 cells. siRNA-ASF1B was revealed to significantly reduce the level of B-cell lymphoma-2 and cyclin D1, and enhance the expression levels of p53, caspase-3 and Bcl-2 associated X protein. Furthermore, the phosphorylation levels of phosphatidylinositol 3 kinase (PI3K) and protein kinase B (Akt) were significantly decreased in the siRNA-ASF1B group compared with the mock group. In summary, the present study demonstrated that silencing of ASF1B suppressed the proliferation, and promoted apoptosis and cell cycle arrest of PCa cells. Inhibition of the PI3K/Akt signaling pathway was pertinent to the role of si-ASF1B. This phenomenon suggests that the downregulation of ASF1B may aid in inhibiting the progression of PCa.

Indexed as

AgedApoptosisCell Cycle ProteinsCell Line, TumorCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMaleMiddle AgedPhosphatidylinositol 3-KinaseProstatic NeoplasmsProto-Oncogene Proteins c-aktASF1B protein, humanCell Cycle ProteinsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-akt

Identifiers

PMID30132513
PMCPMC6192734
OpenAlexW2885593912

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.