Evidence map›Paper›PMID 28460467›Full record

ArticleOncotarget2017

Luteolin inhibits cell proliferation and induces cell apoptosis via down-regulation of mitochondrial membrane potential in esophageal carcinoma cells EC1 and KYSE450.

Ping Chen, Jing-Yang Zhang, Bei-Bei Sha, Yan-Er Ma, Tao Hu, Yang-Cheng Ma, Hao Sun, Jian-Xiang Shi, Zi-Ming Dong, Pei Li

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 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

45 citing papers in PubMed, 73 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

10 authors at 1 institution in 1 country.

Ping ChenCancer Chemoprevention Collaborative Innovation Center in Henan Province, Zhengzhou University, Zhengzhou, Henan, 450001, China.
Jing-Yang ZhangCancer Chemoprevention Collaborative Innovation Center in Henan Province, Zhengzhou University, Zhengzhou, Henan, 450001, China.
Bei-Bei ShaCancer Chemoprevention Collaborative Innovation Center in Henan Province, Zhengzhou University, Zhengzhou, Henan, 450001, China.
Yan-Er MaCancer Chemoprevention Collaborative Innovation Center in Henan Province, Zhengzhou University, Zhengzhou, Henan, 450001, China.
Tao HuCancer Chemoprevention Collaborative Innovation Center in Henan Province, Zhengzhou University, Zhengzhou, Henan, 450001, China.
Yang-Cheng MaCancer Chemoprevention Collaborative Innovation Center in Henan Province, Zhengzhou University, Zhengzhou, Henan, 450001, China.
Hao SunCollege of Public Health, Henan Key Laboratory for Tumor Epidemiology, Affiliated Tumor Hospital, Zhengzhou University, Zhengzhou, Henan, 450001, China.
Jian-Xiang ShiCollege of Public Health, Henan Key Laboratory for Tumor Epidemiology, Affiliated Tumor Hospital, Zhengzhou University, Zhengzhou, Henan, 450001, China.
Zi-Ming DongCancer Chemoprevention Collaborative Innovation Center in Henan Province, Zhengzhou University, Zhengzhou, Henan, 450001, China.
Pei LiCancer Chemoprevention Collaborative Innovation Center in Henan Province, Zhengzhou University, Zhengzhou, Henan, 450001, China.
Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In current study, we investigated the anti-tumor effect of luteolin in human ESCC cell lines in vitro and in vivo and tried to explore the potential mechanisms. Results from flow cytometry showed that luteolin could induce apoptosis and caspase-3 activation and induce cell cycle arrest at G2/M phase in a dose- and time-dependent manner in EC1 and KYSE450 cells. JC-1 test results showed that membrane potential of mitochondria after luteolin treatment was down-regulated and this was an indicator for intrinsic apoptosis. Western Blot results showed the expression of cell cycle regulatory protein p21 and p53 increased and three apoptosis related proteins that participate in mitochondrial apoptotic pathway, namely, Bim, CYT-c and cPARP, also increased in luteolin treated cells compared with control groups. We further confirmed that luteolin could significantly inhibit the growth of ESCC tumors in xenograft mouse models and no evidence of systemic toxicity was observed. Our results suggest that luteolin can induce cell apoptosis and cell cycle arrest in G2/M phase through mitochondrial pathway in EC1 and KYSE450 cell lines and proper utilization of luteolin might be a practical approach in ESCC chemotherapy.

Indexed as

AnimalsApoptosisBcl-2-Like Protein 11Caspase 3Cell CycleCell Cycle CheckpointsCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21Disease Models, AnimalEsophageal NeoplasmsFemaleGene Expression Regulation, NeoplasticHumansLuteolinMembrane Potential, MitochondrialBcl-2-Like Protein 11Caspase 3Cyclin-Dependent Kinase Inhibitor p21LuteolinPoly(ADP-ribose) PolymerasesTumor Suppressor Protein p53cell proliferationchemotherapyesophageal squamous carcinomaluteolinmitochondrial membrane potential

Identifiers

PMID28460467
PMCPMC5432349
OpenAlexW2591743873

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.