Evidence map›Paper›PMID 26682731›Full record

ArticlePloS one2015

Antitumor Effects and Mechanism of Novel Emodin Rhamnoside Derivatives against Human Cancer Cells In Vitro.

Jie-yu Xing, Gao-peng Song, Jun-peng Deng, Ling-zhi Jiang, Ping Xiong, Bin-jie Yang, Shan-shan Liu

Open access · goldAbstract read
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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  11. Health-Promoting Role ofMicroorganisms · 2021
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  13. Glycoconjugation: An approach to cancer therapeutics.World journal of clinical oncology · 2020
    Review
  14. 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 2 countries.

Jie-yu XingDepartment of Pharmaceutical Engineering, South China Agricultural University, Guangzhou, Guangdong, China.
Gao-peng SongDepartment of Pharmaceutical Engineering, South China Agricultural University, Guangzhou, Guangdong, China.
Jun-peng DengDepartment of Biochemistry and Molecular Biology, Oklahoma State University, Stillwater, Oklahoma, United States of America.
Ling-zhi JiangCollege of Life Science, Shenzhen Key Laboratory of Microbial Genetic Engineering, Shenzhen University, Shenzhen, Guangdong, China.
Ping XiongDepartment of Pharmaceutical Engineering, South China Agricultural University, Guangzhou, Guangdong, China.
Bin-jie YangDepartment of Pharmaceutical Engineering, South China Agricultural University, Guangzhou, Guangdong, China.
Shan-shan LiuDepartment of Pharmaceutical Engineering, South China Agricultural University, Guangzhou, Guangdong, China.
South China Agricultural University · CNOklahoma State University · USShenzhen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A series of novel anthracene L-rhamnopyranosides compounds were designed and synthesized and their anti-proliferative activities on cancer cell lines were investigated. We found that one derivative S-8 (EM-d-Rha) strongly inhibited cell proliferation of a panel of different human cancer cell lines including A549, HepG2, OVCAR-3, HeLa and K562 and SGC-790 cell lines, and displayed IC50 values in low micro-molar ranges, which are ten folds more effective than emodin. In addition, we found EM-d-Rha (3-(2",3"-Di-O-acetyl-α-L-rhamnopyranosyl-(1→4)-2',3'-di-O-acetyl-α-L-rhamnopyranosyl)-emodin) substantially induced cellular apoptosis of HepG2 and OVCAR-3 cells in the early growth stage. Furthermore, EM-d-Rha led to the decrease of mitochondrial transmembrane potential, and up-regulated the express of cells apoptosis factors in a concentration- and time-dependent manner. The results indicated the EM-d-Rha may inhibit the growth and proliferation of HepG2 cells through the pathway of apoptosis induction, and the possible molecular mechanism may due to the activation of intrinsic apoptotic signal pathway.

Indexed as

Antineoplastic AgentsCell Line, TumorCell ProliferationCell SurvivalDose-Response Relationship, DrugDrug Screening Assays, AntitumorEmodinGene Expression Regulation, NeoplasticHeLa CellsHep G2 CellsHumansIn Vitro TechniquesMCF-7 CellsMembrane Potential, MitochondrialNeoplasmsAntineoplastic AgentsEmodin

Identifiers

PMID26682731
PMCPMC4684281
OpenAlexW2212021512

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.