Evidence map›Paper›PMID 29344672›Full record

ArticleMolecular medicine reports2018

Histone deacetylase inhibitor trichostatin A and autophagy inhibitor chloroquine synergistically exert anti-tumor activity in H-ras transformed breast epithelial cells.

Liang Gao, Xin Sun, Qi Zhang, Xiaochen Chen, Tongwei Zhao, Liqing Lu, Jianbin Zhang, Yupeng Hong

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 22 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

8 authors at 3 institutions in 1 country.

Liang Gao *Department of Oncology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang 310014, P.R. China.
Xin Sun *Department of Oncology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang 310014, P.R. China.
Qi ZhangDepartment of Hepatobiliary and Pancreatic Surgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310002, P.R. China.
Xiaochen ChenDepartment of Oncology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang 310014, P.R. China.
Tongwei ZhaoDepartment of Oncology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang 310014, P.R. China.
Liqing LuDepartment of Oncology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang 310014, P.R. China.
Jianbin ZhangDepartment of Oncology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang 310014, P.R. China.
Yupeng HongDepartment of Oncology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang 310014, P.R. China.
Hangzhou Medical College · CNZhejiang Provincial People's Hospital · CNSecond Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylase inhibitors (HDACIs) cause oncogene‑transformed mammalian cell death. Our previous study indicated that HDACIs activate forkhead box O1 (FOXO1) and induce autophagy in liver and colon cancer cells. However, whether FOXO1 is involved in HDACI‑mediated oncogene‑transformed mammalian cell death remains unclear. In the present study, H‑ras transformed MCF10A cells were used to investigate the role of FOXO1 in this pathway. Results showed that trichostatin A (TSA), a HDACI, activated apoptosis in MCF10A‑ras cells, but not in MCF10A cells. Furthermore, TSA activated FOXO1 via P21 upregulation, whereas the knockdown of FOXO1 reduced TSA‑induced cell death. In addition, TSA induced autophagy in MCF10A and MCF10A‑ras cells by blocking the mammailian target of rapamycin signaling pathway. Furthermore, autophagy inhibition lead to higher MCF10A‑ras cell death by TSA, thus indicating that autophagy is essential in cell survival. Taken together, the present study demonstrated that TSA causes oncogene‑transformed cell apoptosis via activation of FOXO1 and HDACI‑mediated autophagy induction, which served as important cell survival mechanisms. Notably, the present findings imply that a combination of HDACIs and autophagy inhibitors produce a synergistic anticancer effect.

Indexed as

Antineoplastic AgentsApoptosisAutophagyCell Line, TransformedChloroquineDrug CombinationsDrug SynergismEpithelial CellsForkhead Box Protein O1Gene Expression RegulationHistone Deacetylase InhibitorsHumansHydroxamic AcidsMammary Glands, HumanProto-Oncogene Proteins p21(ras)RNA, Small InterferingAntineoplastic AgentsChloroquineDrug CombinationsForkhead Box Protein O1FOXO1 protein, humanHistone Deacetylase InhibitorsHRAS protein, humanHydroxamic AcidsMTOR protein, humanProto-Oncogene Proteins p21(ras)RNA, Small InterferingTOR Serine-Threonine Kinasestrichostatin Aapoptosisautophagychloroquinehistone deacetylase inhibitorMCF10A-ras cellstrichostatin A

Identifiers

PMID29344672
PMCPMC5802205
OpenAlexW2787851578

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.