Evidence map›Paper›PMID 28518146›Full record

ArticleCell death & disease2017

Acyl-CoA thioesterase 7 is involved in cell cycle progression via regulation of PKCζ-p53-p21 signaling pathway.

Seung Hee Jung, Hyung Chul Lee, Hyun Jung Hwang, Hyun A Park, Young-Ah Moon, Bong Cho Kim, Hyeong Min Lee, Kwang Pyo Kim, Yong-Nyun Kim, Byung Lan Lee and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

38 citing papers in PubMed, 51 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

14 authors at 6 institutions in 1 country.

Seung Hee JungDepartment of Molecular Medicine, Inha University College of Medicine, Incheon, Korea.
Hyung Chul LeeDepartment of Molecular Medicine, Inha University College of Medicine, Incheon, Korea.
Hyun Jung HwangDepartment of Molecular Medicine, Inha University College of Medicine, Incheon, Korea.
Hyun A ParkDepartment of Molecular Medicine, Inha University College of Medicine, Incheon, Korea.
Young-Ah MoonDepartment of Molecular Medicine, Inha University College of Medicine, Incheon, Korea.
Bong Cho KimDivision of Basic Radiation Bioscience, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Hyeong Min LeeDepartment of Applied Chemistry, College of Applied Science, Kyung Hee University, Yongin, Korea.
Kwang Pyo KimDepartment of Applied Chemistry, College of Applied Science, Kyung Hee University, Yongin, Korea.ORCID 0000-0003-0095-3787
Yong-Nyun KimDivision of Cancer Biology, Research Institute, National Cancer Center, Goyang, Korea.
Byung Lan LeeDepartment of Anatomy, Seoul National University College of Medicine, Seoul, Korea.
Jae Cheol LeeDepartment of Oncology, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Korea.
Young-Gyu KoDivision of Life Sciences, Korea University, Seoul, Korea.
Heon Joo ParkHypoxia-Related Disease Research Center, Inha University College of Medicine, Incheon, Korea.
Jae-Seon LeeDepartment of Molecular Medicine, Inha University College of Medicine, Incheon, Korea.ORCID 0000-0001-6002-5267
Inha University · KRKorea Institute of Radiological and Medical Sciences · KRKorea University · KRKyung Hee University · KRNational Cancer Center · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acyl-CoA thioesterase 7 (ACOT7) is a major isoform of the ACOT family that catalyzes hydrolysis of fatty acyl-CoAs to free fatty acids and CoA-SH. However, canonical and non-canonical functions of ACOT7 remain to be discovered. In this study, for the first time, ACOT7 was shown to be responsive to genotoxic stresses such as ionizing radiation (IR) and the anti-cancer drug doxorubicin in time- and dose-dependent manners. ACOT7 knockdown induced cytostasis via activation of the p53-p21 signaling pathway without a DNA damage response. PKCζ was specifically involved in ACOT7 depletion-mediated cell cycle arrest as an upstream molecule of the p53-p21 signaling pathway in MCF7 human breast carcinoma and A549 human lung carcinoma cells. Of the other members of the ACOT family, including ACOT1, 4, 8, 9, 11, 12, and 13 that were expressed in human, ACOT4, 8, and 12 were responsive to genotoxic stresses. However, none of those had a role in cytostasis via activation of the PKCζ-p53-p21 signaling pathway. Analysis of the ACOT7 prognostic value revealed that low ACOT7 levels prolonged overall survival periods in breast and lung cancer patients. Furthermore, ACOT7 mRNA levels were higher in lung cancer patient tissues compared to normal tissues. We also observed a synergistic effect of ACOT7 depletion in combination with either IR or doxorubicin on cell proliferation in breast and lung cancer cells. Together, our data suggest that a low level of ACOT7 may be involved, at least in part, in the prevention of human breast and lung cancer development via regulation of cell cycle progression.

Indexed as

Cell CycleSignal TransductionA549 CellsAntineoplastic AgentsCell Cycle CheckpointsCyclin-Dependent Kinase Inhibitor p21DNA DamageDown-RegulationDoxorubicinDrug SynergismHumansMasoprocolMCF-7 CellsProtein Kinase CProtein Kinase C zetaRadiation, IonizingAntineoplastic AgentsCyclin-Dependent Kinase Inhibitor p21DoxorubicinMasoprocolProtein Kinase CProtein Kinase C zetaThiolester HydrolasesTumor Suppressor Protein p53

Identifiers

PMID28518146
PMCPMC5584527
OpenAlexW2615314534

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.