Evidence map›Paper›PMID 33817118›Full record

ArticleOpen life sciences2018

Emodin Promotes Apoptosis of Human Endometrial Cancer Through Regulating the MAPK and PI3K/ AKT Pathways.

Jun Jiang, Nanyang Zhou, Pian Ying, Ting Zhang, Ruojia Liang, Xuelu Jiang

Open access · goldAbstract read
In one paragraph

Article in Open life sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed, 22 citations in OpenAlex.

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  11. p38β - MAPK11 and its role in female cancers.Journal of ovarian research · 2021
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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 2 institutions in 1 country.

Jun JiangDepartment of gynecology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310006, P. R. China.
Nanyang ZhouDepartment of traditional chinese medicine, Hangzhou Obstetrics & Gynecology Hospital, Hangzhou 310008, P. R. China.
Pian YingDepartment of gynecology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310006, P. R. China.
Ting ZhangDepartment of gynecology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310006, P. R. China.
Ruojia LiangDepartment of gynecology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310006, P. R. China.
Xuelu JiangDepartment of gynecology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310006, P. R. China.
Zhejiang Chinese Medical University · CNHangzhou Hospital of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emodin, a major component of rhubarb, has anti-tumor effects in a variety of cancers, influencing multiple steps of tumor development through modulating several signaling pathways. The aim of this study is to examine the effect of emodin on cell apoptosis and explore the underlying mechanisms in human endometrial cancer cells. Here we report that emodin can inhibit KLE cell proliferation and induce apoptosis in a time- and dose-dependent manner. Western blot assay found that emodin was involved in MAPK and PI3K/Akt signaling pathways. Specifically, emodin significantly suppressed the phosphorylation of AKT, and enhanced the phosphorylation of MAPK pathways. Furthermore, the generation of reactive oxygen species (ROS) was up-regulated in KLE cells upon treatment with emodin, while the anti-oxidant agent N-acetyl cysteine (NAC) can inhibit emodin-induced apoptosis and promote the activation of AKT and Bcl-2. Taken together, we revealed that emodin may induce apoptosis in KLE cells through regulating the PI3K/AKT and MAPK signaling pathways, indicating the importance of emodin as an anti-tumor agent.

Indexed as

apoptosis; MAPKemodinEndometrial cancerPI3K/AKT

Identifiers

PMID33817118
PMCPMC7874679
OpenAlexW2910051162

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.