Evidence map›Paper›PMID 29581836›Full record

ArticleOncotarget2018

RUNX1 and RUNX3 protect against YAP-mediated EMT, stem-ness and shorter survival outcomes in breast cancer.

Madhura Kulkarni, Tuan Zea Tan, Nurfarhanah Bte Syed Sulaiman, John M Lamar, Prashali Bansal, Jianzhou Cui, Yiting Qiao, Yoshiaki Ito

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 73 citations in OpenAlex.

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  4. RUNX1-deficiency drives immune-active ERbioRxiv : the preprint server for biology · 2026
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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

8 authors at 4 institutions in 4 countries.

Madhura KulkarniCancer Science Institute, NUS, Singapore.
Tuan Zea TanCancer Science Institute, NUS, Singapore.
Nurfarhanah Bte Syed SulaimanCancer Science Institute, NUS, Singapore.
John M LamarKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA.
Prashali BansalCancer Science Institute, NUS, Singapore.
Jianzhou CuiCancer Science Institute, NUS, Singapore.
Yiting QiaoCancer Science Institute, NUS, Singapore.
Yoshiaki ItoCancer Science Institute, NUS, Singapore.
National University Cancer Institute, Singapore · SGDuke-NUS Medical School · SGMassachusetts Institute of Technology · USPrashanti Cancer Care Mission · IN

Funding

Tumor Cell Networks CenterU54CA112967 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LAUFFENBURGER, DOUGLAS A · 2004 to 2015
$26.2M
The Extracellular Matrix in Tumor Progression and MetastasisU54CA163109 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI HYNES, RICHARD O · 2011 to 2015
$3.7M
NCI NIH HHS U54 CA112967NCI NIH HHS U54 CA163109
6 · The paper itself

Abstract

Hippo pathway target, YAP has emerged as an important player in solid tumor progression. Here, we identify RUNX1 and RUNX3 as novel negative regulators of oncogenic function of YAP in the context of breast cancer. RUNX proteins are one of the first transcription factors identified to interact with YAP. RUNX1 or RUNX3 expression abrogates YAP-mediated pro-tumorigenic properties of mammary epithelial cell lines in an interaction dependent manner. RUNX1 and RUNX3 inhibit YAP-mediated migration and stem-ness properties of mammary epithelial cell lines by co-regulating YAP-mediated gene expression. Analysis of whole genome expression profiles of breast cancer samples revealed significant co-relation between YAP-RUNX1/RUNX3 expression levels and survival outcomes of breast cancer patients. High RUNX1/RUNX3 expression proved protective towards YAP-dependent patient survival outcomes. High YAP in breast cancer patients' expression profiles co-related with EMT and stem-ness gene signature enrichment. High RUNX1/RUNX3 expression along with high YAP reflected lower enrichment of EMT and stem-ness signatures. This antagonistic activity of RUNX1 and RUNX3 towards oncogenic function of YAP identified in mammary epithelial cells as well as in breast cancer expression profiles gives a novel mechanistic insight into oncogene-tumor suppressor interplay in the context of breast cancer progression. The novel interplay between YAP, RUNX1 and RUNX3 and its significance in breast cancer progression can serve as a prognostic tool to predict cancer recurrence.

Indexed as

breast cancerEMTRUNX1 and RUNX3stem-nessYAP

Identifiers

PMID29581836
PMCPMC5865662
OpenAlexW2790117705

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.