Evidence map›Paper›PMID 27152871›Full record

ArticleCell cycle (Georgetown, Tex.)2016

AS160 controls eukaryotic cell cycle and proliferation by regulating the CDK inhibitor p21.

Pianchou Gongpan, Yanting Lu, Fang Wang, Yuhui Xu, Wenyong Xiong

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 27 citations in OpenAlex.

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  8. Astragalus polysaccharides decrease proliferation, migration, and invasion but increase apoptosis of human osteosarcoma cells by up-regulation of microRNA-133a.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018
    Article
  9. Molecules (Basel, Switzerland) · 2018
    Article
  10. Article
  11. Experimental and therapeutic medicine · 2017
    Article
  12. Article
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

5 authors at 3 institutions in 1 country.

Pianchou Gongpana State Key Laboratory of Phytochemistry and Plant Resources in West China, Kunming Institute of Botany , Chinese Academy of Sciences , Kunming , Yunnan , P.R. China.
Yanting Lua State Key Laboratory of Phytochemistry and Plant Resources in West China, Kunming Institute of Botany , Chinese Academy of Sciences , Kunming , Yunnan , P.R. China.
Fang Wanga State Key Laboratory of Phytochemistry and Plant Resources in West China, Kunming Institute of Botany , Chinese Academy of Sciences , Kunming , Yunnan , P.R. China.
Yuhui Xua State Key Laboratory of Phytochemistry and Plant Resources in West China, Kunming Institute of Botany , Chinese Academy of Sciences , Kunming , Yunnan , P.R. China.
Wenyong Xionga State Key Laboratory of Phytochemistry and Plant Resources in West China, Kunming Institute of Botany , Chinese Academy of Sciences , Kunming , Yunnan , P.R. China.
Chinese Academy of Sciences · CNUniversity of Chinese Academy of Sciences · CNKunming Institute of Botany · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AS160 (TBC1D4) has been implicated in multiple biological processes. However, the role and the mechanism of action of AS160 in the regulation of cell proliferation remain unclear. In this study, we demonstrated that AS160 knockdown led to blunted cell proliferation in multiple cell types, including fibroblasts and cancer cells. The results of cell cycle analysis showed that these cells were arrested in the G1 phase. Intriguingly, this inhibition of cell proliferation and the cell cycle arrest caused by AS160 depletion were glucose independent. Moreover, AS160 silencing led to a marked upregulation of the expression of the cyclin-dependent kinase inhibitor p21. Furthermore, whereas AS160 overexpression resulted in p21 downregulation and rescued the arrested cell cycle in AS160-depeleted cells, p21 silencing rescued the inhibited cell cycle and proliferation in the cells. Thus, our results demonstrated that AS160 regulates glucose-independent eukaryotic cell proliferation through p21-dependent control of the cell cycle, and thereby revealed a molecular mechanism of AS160 modulation of cell cycle and proliferation that is of general physiological significance.

Indexed as

Cell CycleAnimalsCell Cycle CheckpointsCell LineCell ProliferationCyclin-Dependent Kinase Inhibitor p21Eukaryotic CellsG1 PhaseGene Knockdown TechniquesGene SilencingGlucoseGTPase-Activating ProteinsHumansLactic AcidMiceRNA, Small InterferingCyclin-Dependent Kinase Inhibitor p21GlucoseGTPase-Activating ProteinsLactic AcidRNA, Small InterferingTBC1D4 protein, humanTbc1d4 protein, mouseAS160/TBC1D4cell cyclecell proliferationG1/Sp21

Identifiers

PMID27152871
PMCPMC4957568
OpenAlexW2346614495

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.