Evidence map›Paper›PMID 26196392›Full record

ArticlePloS one2015

Metformin Induced AMPK Activation, G0/G1 Phase Cell Cycle Arrest and the Inhibition of Growth of Esophageal Squamous Cell Carcinomas In Vitro and In Vivo.

Xianbin Cai, Xi Hu, Xiaojun Tan, Weijie Cheng, Qinjia Wang, Xiaofeng Chen, Yinghong Guan, Chong Chen, Xubin Jing

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 89 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

9 authors at 3 institutions in 1 country.

Xianbin CaiDepartment of Gastroenterology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515031, China.
Xi HuDepartment of Gastroenterology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515031, China.
Xiaojun TanDepartment of Internal Medicine, Chancheng District Central Hospital, Foshan, Guangdong 528031, China.
Weijie ChengDepartment of Gastroenterology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515031, China.
Qinjia WangDepartment of Gastroenterology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515031, China.
Xiaofeng ChenDepartment of Gastroenterology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515031, China.
Yinghong GuanDepartment of Gastroenterology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515031, China.
Chong ChenDepartment of Gastroenterology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515031, China.
Xubin JingDepartment of Gastroenterology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515031, China.
First Affiliated Hospital of Shantou University Medical College · CNShantou University · CNXian Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Esophageal squamous cell carcinomas (ESCC) have become a severe threat to health and the current treatments for ESCC are frequently not effective. Recent epidemiological studies suggest that the anti-hyperglycemic agent metformin may reduce the risk of developing cancer, including ESCC, among diabetic patients. However, the antitumor effects of metformin on ESCC and the mechanisms underlying its cell cycle regulation remain elusive. The findings reported herein show that the anti-proliferative action of metformin on ESCC cell lines is partially mediated by AMPK. Moreover, we observed that metformin induced G0/G1 phase arrest accompanied by the up-regulation of p21CIP1 and p27KIP1. In vivo experiments further showed that metformin inhibited tumor growth in a ESCC xenograft model. Most importantly, the up-regulation of AMPK, p53, p21CIP1, p27KIP1 and the down-regulation of cyclinD1 are involved in the anti-tumor action of metformin in vivo. In conclusion, metformin inhibits the growth of ESCC cells both in cell cultures and in an animal model. AMPK, p53, p21CIP1, p27KIP1 and cyclinD1 are involved in the inhibition of tumor growth that is induced by metformin and cell cycle arrest in ESCC. These findings indicate that metformin has the potential for use in the treatment of ESCC.

Indexed as

AMP-Activated Protein KinasesAnimalsBlotting, WesternCarcinoma, Squamous CellCell Line, TumorCell ProliferationCell SurvivalCyclin D1Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Enzyme ActivationEsophageal NeoplasmsG1 Phase Cell Cycle CheckpointsHumansHypoglycemic AgentsMaleAMP-Activated Protein KinasesCDKN1A protein, humanCDKN1B protein, humanCyclin D1Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Hypoglycemic AgentsMetforminTumor Suppressor Protein p53

Identifiers

PMID26196392
PMCPMC4510392
OpenAlexW2283275285

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.