Evidence map›Paper›PMID 27429851›Full record

ArticleAmerican journal of cancer research2016

Synergistic reversal effect of epithelial-to-mesenchymal transition by miR-223 inhibitor and genistein in gemcitabine-resistant pancreatic cancer cells.

Jia Ma, Fanpeng Zeng, Cong Ma, Haijie Pang, Binbin Fang, Chaoqun Lian, Bin Yin, Xueping Zhang, Zhiwei Wang, Jun Xia

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

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  4. Cellular and Molecular Mechanisms Modulated by Genistein in Cancer.International journal of molecular sciences · 2025
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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 4 institutions in 2 countries.

Jia MaThe Cyrus Tang Hematology Center and Collaborative Innovation Center of Hematology, Jiangsu Institute of Hematology, The First Affiliated Hospital, Soochow UniversitySuzhou 215123, China; Department of Biochemistry and Molecular Biology, Bengbu Medical CollegeAnhui 233030, China.
Fanpeng ZengResearch Center of Clinical Laboratory Science, Bengbu Medical College Anhui 233030, China.
Cong MaResearch Center of Clinical Laboratory Science, Bengbu Medical College Anhui 233030, China.
Haijie PangResearch Center of Clinical Laboratory Science, Bengbu Medical College Anhui 233030, China.
Binbin FangResearch Center of Clinical Laboratory Science, Bengbu Medical College Anhui 233030, China.
Chaoqun LianDepartment of Biochemistry and Molecular Biology, Bengbu Medical College Anhui 233030, China.
Bin YinThe Cyrus Tang Hematology Center and Collaborative Innovation Center of Hematology, Jiangsu Institute of Hematology, The First Affiliated Hospital, Soochow University Suzhou 215123, China.
Xueping ZhangDepartment of Anesthesiology, Shenzhen People's Hospital, 2nd Clinical Medical College of Jinan University Shenzhen 518020, China.
Zhiwei WangThe Cyrus Tang Hematology Center and Collaborative Innovation Center of Hematology, Jiangsu Institute of Hematology, The First Affiliated Hospital, Soochow UniversitySuzhou 215123, China; Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical SchoolBoston, MA 02215, USA.
Jun XiaDepartment of Biochemistry and Molecular Biology, Bengbu Medical College Anhui 233030, China.
Bengbu Medical College · CNSoochow University · CNBeth Israel Deaconess Medical Center · USShenZhen People’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging studies have demonstrated that EMT phenotype is closely related with tumor progression and drug resistance in a variety of human cancers. Recently, it has been extensively demonstrated that microRNAs (miRNAs) play a pivotal role in regulating EMT. In our previously reports, we have reported that inhibition of miR-223 could reverse EMT phenotype and improve chemotherapeutic drug sensitivity. We also reported that genistein down-regulated miR-223 expression in gemcitabine-resistant (GR) pancreatic cancer cells. Here, we explored whether there was the synergistic effect between miR-223 inhibitor and genistein on cell growth, migration, invasion and reversal of EMT in GR pancreatic cancer. We found that the combination of miR-223 inhibitor and genistein synergistically reduced cell motility and invasion and enhanced gemcitabine sensitivity in GR cells. In addition, we further observed that miR-223 inhibitor and genistein reversed EMT features in GR cells. This study suggests that the combination of miR-223 inhibitor and genistein may be a potential therapeutic strategy for the treatment of pancreatic cancer.

Indexed as

EMTGemcitabinegenisteininvasionmiR-223pancreatic cancer

Identifiers

PMID27429851
PMCPMC4937740
OpenAlexW2502640854

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.