Evidence map›Paper›PMID 22159556›Full record

ArticleInternational journal of oncology2012

Emodin reverses gemcitabine resistance in pancreatic cancer cells via the mitochondrial apoptosis pathway in vitro.

Dian-Lei Liu, Heqi Bu, Hong Li, Hui Chen, Hong-Chun Guo, Zhao-Hong Wang, Hong-Fei Tong, Zhong-Lin Ni, Hai-Bin Liu, Sheng-Zhang Lin

Open access · bronzeAbstract read
In one paragraph

Article in International journal of oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.3field-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

26 citing papers in PubMed, 54 citations in OpenAlex.

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  11. Comparative study amongSaudi journal of biological sciences · 2022
    Article
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  15. An Update of Anthraquinone Derivatives Emodin, Diacerein, and Catenarin in Diabetes.Evidence-based complementary and alternative medicine : eCAM · 2021
    Review
  16. Emodin-Conjugated PEGylation of FeInternational journal of nanomedicine · 2021
    Article
  17. Review
  18. Review
  19. 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

10 authors at 2 institutions in 1 country.

Dian-Lei LiuDepartment of Surgery, The Second Affiliated Hospital of Wenzhou Medical College, No 109, West Xue-yuan Road, Wenzhou 325027, PR China.
Heqi Bu
Hong Li
Hui Chen
Hong-Chun Guo
Zhao-Hong Wang
Hong-Fei Tong
Zhong-Lin Ni
Hai-Bin Liu
Sheng-Zhang Lin
Wenzhou Medical University · CNWenzhou Vocational College of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gemcitabine resistance is a common problem of pancreatic cancer chemotherapy, and how to reverse it plays an important role in the treatment of pancreatic cancer. This study investigated the effect of emodin on the gemcitabine-resistant pancreatic cancer cell line SW1990/Gem, and explored the potential mechanism of its action. SW1990/Gem was obtained by culture of the pancreatic cancer cell line SW1990 in vitro by intermittently increasing the concentration of gemcitabine in the culture medium for 10 months, observing the morphology using inverted microscopy. SW1990/Gem cells were pretreated with emodin (10 µM) for different periods followed by treatment with gemcitabine (20 µM) for 48 h; cell proliferation was tested by MTT assay. SW1990/Gem cells were treated by emodin with different concentrations for 48 h, cell apoptosis was detected by flow cytometry (FCM). The expression of gene and protein, such as MDR-1 (P-gp), NF-κB, Bcl-2, Bax, cytochrome-C (cytosol), caspase-9 and -3 were measured by RT-PCR and Western blotting. The function of P-gp in SW1990/Gem cells was checked by FCM. The results showed that the SW1990/Gem cells changed greatly in morphology and the resistance index was 48.63. Emodin promoted cell apoptosis of the gemcitabine-resistant cell line SW1990/Gem in a dose-dependent manner. Emodin enhanced the SW1990/Gem cell sensitivity to gemcitabine in a time-dependent manner. Emodin monotherapy or combination with gemcitabine both decreased the gene and protein expression levels of MDR-1 (P-gp), NF-κB and Bcl-2 and inhibited the function of P-gp, but increased the expression levels of Bax, cytochrome-C (cytosol), caspase-9 and -3, and promoted cell apoptosis. This demonstrated that emodin had a reversing effect on the gemcitabine-resistant cell line SW1990/Gem, possibly via decreasing the function of P-gp and activating the mitochondrial apoptosis pathway in vitro.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsApoptosisCell Growth ProcessesCell Line, TumorDeoxycytidineDrug Resistance, NeoplasmDrug SynergismEmodinGemcitabineHumansMitochondriaPancreatic NeoplasmsProtein Kinase InhibitorsDeoxycytidineEmodinGemcitabineProtein Kinase Inhibitors

Identifiers

PMID22159556
PMCPMC3584653
OpenAlexW2160234260

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.