Evidence map›Paper›PMID 24521357›Full record

ArticleBMC cancer2014

MiR-200a inhibits epithelial-mesenchymal transition of pancreatic cancer stem cell.

Yuhua Lu, Jingjing Lu, Xiaohong Li, Hui Zhu, Xiangjun Fan, Shajun Zhu, Yao Wang, Qingsong Guo, Lei Wang, Yan Huang and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
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  3. Article
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  6. Pancreatic cancer stemness: dynamic status in malignant progression.Journal of experimental & clinical cancer research : CR · 2023
    Review
  7. Article
  8. Development of 5-FU-modified tumor suppressor microRNAs as a platform for novel microRNA-based cancer therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  9. microRNA-21 Regulates Stemness in Pancreatic Ductal Adenocarcinoma Cells.International journal of molecular sciences · 2022
    Article
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  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

12 authors at 3 institutions in 2 countries.

Yuhua Lu
Jingjing Lu
Xiaohong Li
Hui Zhu
Xiangjun Fan
Shajun Zhu
Yao Wang
Qingsong Guo
Lei Wang
Yan Huang
Mingyan ZhuDepartment of General Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province 226001, P, R, China. zmy5661@163.com.
Zhiwei Wang
Affiliated Hospital of Nantong University · CNNantong University · CNForest Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPancreatic cancer is one of the most aggressive cancers, and the aggressiveness of pancreatic cancer is in part due to its intrinsic and extrinsic drug resistance characteristics, which are also associated with the acquisition of epithelial-to-mesenchymal transition (EMT). Increasing evidence suggests that EMT-type cells share many biological characteristics with cancer stem-like cells. And miR-200 has been identified as a powerful regulator of EMT.

methodsCancer Stem Cells (CSCs) of human pancreatic cancer cell line PANC-1 were processed for CD24, CD44 and ESA multi-colorstaining, and sorted out on a BD FACS Aria II machine. RT-qPCR was performed using the miScript PCR Kit to assay the expression of miR-200 family. In order to find the role of miR-200a in the process of EMT, miR-200a mimic was transfected to CSCs.

resultsPancreatic cancer cells with EMT phenotype displayed stem-like cell features characterized by the expression of cell surface markers CD24, CD44 and epithelial-specific antigen (ESA), which was associated with decreased expression of miR-200a. Moreover, overexpression of miR-200a was resulted in down-regulation of N-cadherin, ZEB1 and vimentin, but up-regulation of E-cadherin. In addition, miR-200a overexpression inhibited cell migration and invasion in CSCs.

conclusionIn our study, we found that miR-200a played an important role in linking the characteristics of cancer stem-like cells with EMT-like cell signatures in pancreatic cancer. Selective elimination of cancer stem-like cells by reversing the EMT phenotype to mesenchymal-to-epithelial transition (MET) phenotype using novel agents would be useful for prevention and/or treatment of pancreatic cancer.

Indexed as

Cell Line, TumorCell MovementEpithelial-Mesenchymal TransitionFlow CytometryHumansMicroRNAsNeoplastic Stem CellsPancreatic NeoplasmsMicroRNAsMIRN200 microRNA, human

Identifiers

PMID24521357
PMCPMC3923443
OpenAlexW2140737952

What OpenQuestion holds

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LicenceCC BY
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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.