Evidence map›Paper›PMID 27409663›Full record

ArticleOncotarget2016

Histone deacetylase inhibitors regulate P-gp expression in colorectal cancer via transcriptional activation and mRNA stabilization.

Hao Wang, Cheng Huang, Liang Zhao, Huan Zhang, Jing Mo Yang, Peng Luo, Bing-Xiang Zhan, Qing Pan, Jun Li, Bao-Long Wang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  7. Activation ofCancers · 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

10 authors at 3 institutions in 1 country.

Hao WangDepartment of Clinical Laboratory, Affiliated Provincial Hospital of Anhui Medical University, Hefei, China.
Cheng HuangSchool of Pharmacy, Anhui Medical University, Hefei, China.
Liang ZhaoDepartment of Clinical Laboratory, Affiliated Provincial Hospital of Anhui Medical University, Hefei, China.
Huan ZhangDepartment of Biochemistry and Molecular Biology, Sichuan Cancer Hospital and Institute, Chengdu, China.
Jing Mo YangDepartment of Pharmacy, Anhui Provincial Cancer Hospital, West Branch of Anhui Provincial Hospital, Hefei, China.
Peng LuoDepartment of Clinical Laboratory, Affiliated Provincial Hospital of Anhui Medical University, Hefei, China.
Bing-Xiang ZhanDepartment of Clinical Laboratory, Affiliated Provincial Hospital of Anhui Medical University, Hefei, China.
Qing PanDepartment of Clinical Laboratory, Affiliated Provincial Hospital of Anhui Medical University, Hefei, China.
Jun LiSchool of Pharmacy, Anhui Medical University, Hefei, China.
Bao-Long WangDepartment of Clinical Laboratory, Affiliated Provincial Hospital of Anhui Medical University, Hefei, China.
Anhui Medical University · CNAnhui Provincial Hospital · CNSichuan Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylase inhibitors (HDACIs) are emerging as a novel class of anti-tumor drugs. But the effect of HDACIs in tumors treatment has been disappointing, which mainly due to the acquisition of resistance to HDACIs. However, the underlying mechanisms have not been clearly understood. In this study, it was found that HDACIs SAHA and TSA increased P-gp expression in CRC cells, which has been well known to contribute to drug resistant. The mechanisms underlying these effects were investigated. We showed that HDACIs enhanced transcriptional activity of P-gp protein encoding gene ABCB1. HDACIs treatment also increased the protein and mRNA expression of STAT3, but not PXR, CAR, Foxo3a or β-catenin, which are known to be involved in ABCB transcription regulation. Interestingly, knockdown of STAT3 significantly attenuated HDACIs-induced P-gp up-regulation in colorectal cancer cells, suggesting that STAT3 plays a crucial role in HDACIs-up-regulated P-gp. Furthermore, this study revealed for the first time that HDACIs enhanced the stability of ABCB1 at post-transcriptional level. Taken together, these results proved that HDACIs induced P-gp expression by two distinct ways, transcriptional activation and mRNA stabilization. Our results suggested that more attention should be paid to the cancer treatment using HDACIs since they will induce multidrug resistance in cancer cells.

Indexed as

Gene Expression Regulation, NeoplasticTranscriptional ActivationATP Binding Cassette Transporter, Subfamily Bbeta CateninCell Line, TumorColorectal NeoplasmsDrug Resistance, MultipleDrug Resistance, NeoplasmForkhead Box Protein O3HCT116 CellsHistone Deacetylase InhibitorsHumansRNA InterferenceRNA, MessengerSTAT3 Transcription FactorABCB1 protein, humanATP Binding Cassette Transporter, Subfamily Bbeta CateninCTNNB1 protein, humanForkhead Box Protein O3FOXO3 protein, humanHistone Deacetylase InhibitorsRNA, MessengerSTAT3 protein, humanSTAT3 Transcription Factorhistone deacetylase inhibitorsmultidrug resistanceP-gpstabilitySTAT3

Identifiers

PMID27409663
PMCPMC5226552
OpenAlexW2470094136

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.