Evidence map›Paper›PMID 31814524›Full record

ArticleEpigenetics

4-phenylbutyric acid promotes migration of gastric cancer cells by histone deacetylase inhibition-mediated IL-8 upregulation.

Xiaonan Shi, Libao Gong, Yunpeng Liu, Kezuo Hou, Yibo Fan, Ce Li, Ti Wen, Xiujuan Qu, Xiaofang Che

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

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  9. The Potential of Senescence as a Target for Developing Anticancer Therapy.International journal of molecular sciences · 2023
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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

9 authors at 1 institution in 1 country.

Xiaonan ShiDepartment of Medical Oncology, The First Hospital of China Medical University , Shenyang, China.
Libao GongDepartment of Medical Oncology, The First Hospital of China Medical University , Shenyang, China.
Yunpeng LiuDepartment of Medical Oncology, The First Hospital of China Medical University , Shenyang, China.
Kezuo HouDepartment of Medical Oncology, The First Hospital of China Medical University , Shenyang, China.
Yibo FanDepartment of Medical Oncology, The First Hospital of China Medical University , Shenyang, China.
Ce LiDepartment of Medical Oncology, The First Hospital of China Medical University , Shenyang, China.
Ti WenDepartment of Medical Oncology, The First Hospital of China Medical University , Shenyang, China.
Xiujuan QuDepartment of Medical Oncology, The First Hospital of China Medical University , Shenyang, China.
Xiaofang CheDepartment of Medical Oncology, The First Hospital of China Medical University , Shenyang, China.ORCID 0000-0002-9087-1007
First Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone acetylation is regulated by histone acetyltransferases (HATs) and histone deacetylases (HDACs). It is associated with gene transcription and expression. 4-Phenylbutyric acid (4-PBA), an HDAC inhibitor (HDACi), can inhibit cancer cell proliferation by increasing the level of histone acetylation. However, 4-PBA did not show any efficacy in clinical trials. In this study, we found that 4-PBA induced epithelial-mesenchymal transition (EMT) in gastric cancer cell lines MGC-803 and BGC-823 with ectopic E-cadherin expression. Based on the expression profile microarray, IL-8 was the most significantly up-regulated gene by 4-PBA, and was selected for further investigation. Knockdown of IL-8 partially prevented 4-PBA-induced-EMT by blocking the activation of the downstream Gab2-ERK pathway. Furthermore, CHIP assay confirmed that acetyl-H3 directly combined with the promoter region of IL-8 to promote its transcription. Therefore, the results of this study demonstrated that 4-PBA-mediated inhibition of HDAC activity could induce EMT in gastric cancer cells via acetyl-histone-mediated IL-8 upregulation, and the downstream Gab2/ERK activation. These data indicated the possible reason for the failure of 4-PBA in clinical trials.

Indexed as

Antineoplastic AgentsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionHistone Deacetylase InhibitorsHistone DeacetylasesHumansInterleukin-8PhenylbutyratesStomach NeoplasmsUp-Regulation4-phenylbutyric acidAntineoplastic AgentsHistone Deacetylase InhibitorsHistone DeacetylasesInterleukin-8Phenylbutyrates4-PBAEMTgastric cancer cellhistone acetylationhistone deacetylase inhibitorIL-8

Identifiers

PMID31814524
PMCPMC7574398
OpenAlexW2993191941

What OpenQuestion holds

Textmetadata
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.