Evidence map›Paper›PMID 30717766›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

PCK1 negatively regulates cell cycle progression and hepatoma cell proliferation via the AMPK/p27

Lin Tuo, Jin Xiang, Xuanming Pan, Jieli Hu, Hua Tang, Li Liang, Jie Xia, Yuan Hu, Wenlu Zhang, Ailong Huang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Interplay Between Glucose Metabolism and Chromatin Modifications in Cancer.Frontiers in cell and developmental biology · 2021
    Pooled it
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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

12 authors at 1 institution in 1 country.

Lin TuoKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China.
Jin XiangKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China.
Xuanming PanKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China.
Jieli HuKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China.
Hua TangKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China.
Li LiangKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China.
Jie XiaKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China.
Yuan HuKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China.
Wenlu ZhangKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China.
Ailong HuangKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China. ahuang@cqmu.edu.cn.
Kai WangKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China. wangkai@cqmu.edu.cn.
Ni TangKey Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People's Republic of China. nitang@cqmu.edu.cn.
Chongqing Medical University · CN

Funding

Department of S and T for Social Development 2012ZX10002005-003-002Department of S and T for Social Development 2017ZX10202203-004National Natural Science Foundation of China 81471946,81661148057National Natural Science Foundation of China 81572683, 81371827, 81872270,31171307National Natural Science Foundation of China 81602417National Natural Science Foundation of China 81671997Natural Science Foundation of Chongqing cstc2015jcyjBX0011, cstc2018jcyjAX0254
6 · The paper itself

Abstract

backgroundAltered glucose metabolism endows tumor cells with metabolic flexibility for biosynthesis requirements. Phosphoenolpyruvate carboxykinase 1 (PCK1), a key enzyme in the gluconeogenesis pathway, is downregulated in hepatocellular carcinoma (HCC) and predicts poor prognosis. Overexpression of PCK1 has been shown to suppress liver tumor growth, but the underlying mechanism remains unclear.

methodsmRNA and protein expression patterns of PCK1, AMPK, pAMPK, and the CDK/Rb/E2F pathway were determined using qRT-PCR and western blotting. Cell proliferation ability and cell cycle were assessed by MTS assay and flow cytometric analysis. The effect of PCK1 on tumor growth was examined in xenograft implantation models.

resultsBoth gain and loss-of-function experiments demonstrated that PCK1 deficiency promotes hepatoma cell proliferation through inactivation of AMPK, suppression of p27

conclusionThis study revealed that PCK1 negatively regulates cell cycle progression and hepatoma cell proliferation via the AMPK/p27

Indexed as

AMP-Activated Protein KinasesAnimalsCalcium-Binding ProteinsCarcinoma, HepatocellularCell Line, TumorCell ProliferationCyclin-Dependent KinasesDown-RegulationE2F Transcription FactorsG1 Phase Cell Cycle CheckpointsGene Knockdown TechniquesGlucoseHumansHypoglycemic AgentsIntracellular Signaling Peptides and ProteinsLiver NeoplasmsAMP-Activated Protein KinasesCalcium-Binding ProteinsCIB1 protein, humanCyclin-Dependent KinasesE2F Transcription FactorsGlucoseHypoglycemic AgentsIntracellular Signaling Peptides and ProteinsMetforminPCK1 protein, humanPhosphoenolpyruvate Carboxykinase (GTP)AMP-activated protein kinaseCDK/Rb/E2F pathwayCell cycle arrestHepatocellular carcinomaPhosphoenolpyruvate carboxykinase 1

Identifiers

PMID30717766
PMCPMC6360696
OpenAlexW2921283762

What OpenQuestion 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 OpenQuestion graph.