Evidence map›Paper›PMID 28423719›Full record

ArticleOncotarget2017

AMPKα phosphatase Ppm1E upregulation in human gastric cancer is required for cell proliferation.

Min-Bin Chen, Yuan-Yuan Liu, Li-Bo Cheng, Jian-Wei Lu, Ping Zeng, Pei-Hua Lu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. [miR-342-3p Promotes the Proliferation, Migration, and Invasion of Clear Cell Renal Cell Carcinoma Cells by Targeted Inhibition of PPM1E].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024
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  9. The role of TRPV1 ion channels in the suppression of gastric cancer development.Journal of experimental & clinical cancer research : CR · 2020
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  11. Repression of miR-135b-5p promotes metastasis of early-stage breast cancer by regulating downstream target SDCBP.Laboratory investigation; a journal of technical methods and pathology · 2019
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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

6 authors at 5 institutions in 1 country.

Min-Bin ChenDepartment of Radiotherapy and Oncology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, China.
Yuan-Yuan LiuDepartment of Radiotherapy and Oncology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, China.
Li-Bo ChengDepartment of Ophthalmology, Wuxi Second Hospital, Nanjing Medical University, Wu'xi, China.
Jian-Wei LuDepartment of Oncology, Jiangsu Cancer Hospital Affiliated to Nanjing Medical University, Nanjing, China.
Ping ZengDepartment of Radiotherapy and Oncology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, China.
Pei-Hua LuDepartment of Radiotherapy and Oncology, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi, China.
First People's Hospital of Kunshan · CNJiangsu Cancer Hospital · CNJiangsu University · CNNanjing Medical University · CNWuxi People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of AMP-activated protein kinase (AMPK) is a valuable anti-cancer strategy. In the current study, we tested expression and potential function of Ca2+/calmodulin-dependent protein kinase phosphatase (Ppm1E), an AMPKα phosphatase, in human gastric cancers. Ppm1E expression was elevated in human gastric cancer tissues (vs. normal tissues), which was correlated with AMPK (p-AMPKα, Thr-172) dephosphorylation and mTOR complex 1 (mTORC1) activation. Ppm1E upregulation, AMPK inhibition and mTORC1 activation were also observed in human gastric cancer cell lines (AGS, HGC-27, and SNU601). Intriguingly, Ppm1E knockdown by shRNA induced AMPK activation, mTORC1 inactivation, and proliferation inhibition in AGS cells. On the other hand, forced over-expression of Ppm1E induced further AMPK inhibition and mTORC1 activation to enhance AGS cell proliferation. Remarkably, microRNA-135b-5p ("miR-135b-5p"), an anti-Ppm1E microRNA, was downregulated in both human gastric cancer tissues and cells. Reversely, miR-135b-5p exogenous expression caused Ppm1E depletion, AMPK activation, and AGC cell proliferation inhibition. Together, Ppm1E upregulation in human gastric cancer is important for cell proliferation, possible via regulating AMPK-mTOR signaling.

Indexed as

AMP-Activated Protein KinasesCell Line, TumorCell ProliferationCell SurvivalGene ExpressionGene SilencingHumansPhosphorylationProtein Phosphatase 2CSignal TransductionStomach NeoplasmsTOR Serine-Threonine KinasesAMP-Activated Protein KinasesProtein Phosphatase 2CTOR Serine-Threonine KinasesAMPKαgastric cancermiR-135b-5pmTORPpm1E

Identifiers

PMID28423719
PMCPMC5458207
OpenAlexW2593302229

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.