Evidence map›Paper›PMID 26162964›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2015

Anti-tumor effect of emodin on gynecological cancer cells.

Yaoxian Wang, Hui Yu, Jin Zhang, Xin Ge, Jing Gao, Yunyan Zhang, Ge Lou

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. The Invasive SpeciesFrontiers in pharmacology · 2022
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  13. 7-Molecules (Basel, Switzerland) · 2019
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  17. EMODIN DOWNREGULATES CELL PROLIFERATION MARKERS DURING DMBA INDUCED ORAL CARCINOGENESIS IN GOLDEN SYRIAN HAMSTERS.African journal of traditional, complementary, and alternative medicines : AJTCAM · 2017
    Article
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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

7 authors at 3 institutions in 1 country.

Yaoxian WangDepartment of Gynaecology, Harbin Medical University Cancer Hospital, 150 Hapin Road, Harbin, 150081, China.
Hui YuCardiopulmonary Function Room, Harbin Medical University Cancer Hospital, Harbin, China.
Jin ZhangDepartment of Gynaecology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.
Xin GeDepartment of General Surgery, The Provincial Hospital of Heilongjiang, Harbin, China.
Jing GaoDepartment of Gynaecology, Harbin Medical University Cancer Hospital, 150 Hapin Road, Harbin, 150081, China.
Yunyan ZhangDepartment of Gynaecology, Harbin Medical University Cancer Hospital, 150 Hapin Road, Harbin, 150081, China.
Ge LouDepartment of Gynaecology, Harbin Medical University Cancer Hospital, 150 Hapin Road, Harbin, 150081, China. Gexincom@163.com.
Harbin Medical University · CNThird Affiliated Hospital of Harbin Medical University · CNHeilongjiang Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeAlthough an anti-tumor effect of emodin has been reported before, its effect on human gynecological cancer cells has so far not been studied. Here, we assessed the effect of emodin on cervical cancer-derived (Hela), choriocarcinoma-derived (JAR) and ovarian cancer-derived (HO-8910) cells, and investigated the possible underlying molecular and cellular mechanisms. METHODS AND

resultsThe respective cells were treated with 0, 5, 10 or 15 μM emodin for 72 h. Subsequently, MTT and Transwell in vitro migration assays revealed that emodin significantly decreased the viability and invasive capacity of the gynecological cancer-derived cells tested. We found that emodin induced apoptosis and significantly decreased mitochondrial membrane potential and ATP release in these cells. We also found that emodin may exert its apoptotic effects via regulating the activity of caspase-9 and the expression of cleaved-caspase-3. Moreover, we found that emodin induced a cell cycle arrest at the G0/G1 phase, possibly through down-regulating the key cell cycle regulators Cyclin D and Cyclin E. Interestingly, emodin also led to autophagic cell death, as revealed by increased MAP LC3 expression, a marker of the autophagosome, and decreased expression of the autophagy regulators Beclin-1 and Atg12-Atg5. Finally, we found that the protein levels of both VEGF and VEGFR-2 were significantly decreased in emodin-treated cells, suggesting an anti-angiogenic effect of emodin on gynecological cancer-derived cells.

conclusionsOur results suggest that emodin exhibits an anti-tumor effect on gynecological cancer-derived cells, possibly through multiple mechanisms including the induction of apoptosis and autophagy, the arrest of the cell cycle, and the inhibition of angiogenesis. Our findings may provide a basis for the design of potential emodin-based strategies for the treatment of gynecological tumors.

Indexed as

Antineoplastic AgentsApoptosisApoptosis Regulatory ProteinsAutophagyBlotting, WesternCaspase 9Cell Cycle CheckpointsCell MovementCell ProliferationCell SurvivalDose-Response Relationship, DrugEmodinFemaleGene Expression Regulation, NeoplasticGenital Neoplasms, FemaleHeLa CellsAntineoplastic AgentsApoptosis Regulatory ProteinsCaspase 9EmodinKDR protein, humanMAP1LC3A protein, humanMatrix Metalloproteinase 9Microtubule-Associated ProteinsVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2AngiogenesisAnti-tumor effectApoptosisAutophagyCell cycle arrestEmodinGynecological cancer cells

Identifiers

PMID26162964
PMCPMC13004245
OpenAlexW2103724828

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.