Evidence map›Paper›PMID 21057539›Full record

ArticleOncogene2011

Control of EVI-1 oncogene expression in metastatic breast cancer cells through microRNA miR-22.

J B Patel, H N Appaiah, R M Burnett, P Bhat-Nakshatri, G Wang, R Mehta, S Badve, M J Thomson, S Hammond, P Steeg and 2 more

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
3.5field-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

74 citing papers in PubMed, 121 citations in OpenAlex.

  1. Review
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  16. Review
  17. Article
  18. EVI1 as a Marker for Lymph Node Metastasis in HNSCC.International journal of molecular sciences · 2020
    Article
  19. Article
  20. Article

14 more citing papers are in PubMed but not listed here.

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 5 institutions in 1 country.

J B PatelDepartment of Surgery, Indiana University School of Medicine, Indianapolis, IN, USA.
H N Appaiah
R M Burnett
P Bhat-Nakshatri
G Wang
R Mehta
S Badve
M J Thomson
S Hammond
P Steeg
Y Liu
H Nakshatri
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · USNational Cancer Institute · USUNC Lineberger Comprehensive Cancer CenterVanderbilt University · US

Funding

REGULATION OF HEMATOPOIETIC CELL PRODUCTIONT32DK007519 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KAPLAN, MARK H · 1986 to 2020
$7.1M
Cancer Biology Training ProgramT32CA111198 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI NAKSHATRI, HARIKRISHNA · 2005 to 2009
$1.8M
NCI NIH HHS T32 CA111198NIDDK NIH HHS T32 DK07519
6 · The paper itself

Abstract

Metastasis in breast cancer carries a disproportionately worse prognosis than localized primary disease. To identify microRNAs (miRNA) involved in metastasis, the expression of 254 miRNAs was measured across the following cell lines using microarray analysis: MDA-MB-231 breast cancer cells, cells that grew as a tumor in the mammary fat pad of nude mice (TMD-231), metastatic disease to the lungs (LMD-231), bone (BMD-231) and adrenal gland (ADMD-231). A brain-seeking variant of this cell line (231-BR) was used additionally in validation studies. Twenty miRNAs were upregulated and seven were downregulated in metastatic cancer cells compared with TMD-231 cells. The expression of the tumor suppressor miRNAs let-7 and miR-22 was consistently downregulated in metastatic cancer cells. These metastatic cells expressed higher levels of putative/proven miR-22 target oncogenes ERBB3, CDC25C and EVI-1. Introduction of miR-22 into cancer cells reduced the levels of ERBB3 and EVI-1 as well as phospho-AKT, an EVI-1 downstream target. The miR-22 primary transcript is located in the 5'-untranslated region of an open reading frame C17orf91, and the promoter/enhancer of C17orf91 drives miR-22 expression. We observed elevated C17orf91 expression in non-basal subtype compared with basal subtype breast cancers. In contrast, elevated expression of EVI-1 was observed in basal subtype and was associated with poor outcome in estrogen receptor-negative breast cancer patients. These results suggest that metastatic cancer cells increase specific oncogenic signaling proteins through downregulation of miRNAs. Identifying such metastasis-specific oncogenic pathways may help to manipulate tumor behavior and aid in the design of more effective targeted therapies.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBreast NeoplasmsCell Line, TumorDNA-Binding ProteinsFemaleHumansMDS1 and EVI1 Complex Locus ProteinMiceMice, NudeMicroRNAsNeoplasm MetastasisNeoplasm TransplantationOligonucleotide Array Sequence AnalysisProto-OncogenesReceptors, EstrogenDNA-Binding ProteinsMDS1 and EVI1 Complex Locus ProteinMECOM protein, humanMicroRNAsMIRN22 microRNA, humanReceptors, EstrogenTranscription Factors

Identifiers

PMID21057539
OpenAlexW2076814104

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.