Evidence map›Paper›PMID 27563827›Full record

ArticleOncotarget2016

Integrin β1, myosin light chain kinase and myosin IIA are required for activation of PI3K-AKT signaling following MEK inhibition in metastatic triple negative breast cancer.

Cheolwon Choi, Junyeob Kwon, Sunyoung Lim, David M Helfman

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  5. Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024
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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

4 authors at 1 institution in 1 country.

Cheolwon ChoiDepartment of Biological Sciences, Korean Advanced Institute of Science and Technology Daejeon, Korea.
Junyeob KwonDepartment of Biological Sciences, Korean Advanced Institute of Science and Technology Daejeon, Korea.
Sunyoung LimDepartment of Biological Sciences, Korean Advanced Institute of Science and Technology Daejeon, Korea.
David M HelfmanDepartment of Biological Sciences, Korean Advanced Institute of Science and Technology Daejeon, Korea.
Korea Advanced Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The effectiveness of targeted therapies against the Ras-ERK signaling pathway are limited due to adaptive resistance of tumor cells. Inhibition of the Ras-ERK pathway can result in activation of the PI3K-AKT pathway, thereby diminishing the therapeutic effects of targeting ERK signaling. Here we investigated the crosstalk between the Ras-ERK and PI3K-AKT pathways in MDA-MB-231 breast cancer cell lines that have a preference to metastasize to lung (LM2), brain (BrM2) or bone (BoM2). Inhibition of the Ras-ERK pathway reduced motility in both parental and BoM2 cells. In contrast, inhibition of the Ras-ERK pathway in BrM2 and LM2 cells resulted in activation of PI3K-AKT signaling that was responsible for continued cell motility. Analysis of the cross talk between Ras-ERK and PI3K-AKT signaling pathways revealed integrin β1, myosin light chain kinase (MLCK) and myosin IIA are required for the activation of PI3K-AKT following inhibition of the Ras-ERK pathway. Furthermore, feedback activation of the PI3K-AKT pathway following MEK suppression was independent of the epidermal growth factor receptor. Thus, integrin β1, MLCK, and myosin IIA are factors in the development of resistance to MEK inhibitors. These proteins could provide an opportunity to develop markers and therapeutic targets in a subgroup of triple negative breast cancer (TNBC) that exhibit resistance against MEK inhibition.

Indexed as

ApoptosisBiomarkers, TumorBone NeoplasmsBrain NeoplasmsCell MovementCell ProliferationFemaleHumansIntegrin beta1MAP Kinase Kinase 1Myosin-Light-Chain KinaseNonmuscle Myosin Type IIAPhosphatidylinositol 3-KinasesPhosphorylationProtein Kinase InhibitorsProto-Oncogene Proteins c-aktBiomarkers, TumorIntegrin beta1MAP2K1 protein, humanMAP Kinase Kinase 1Myosin-Light-Chain KinaseNonmuscle Myosin Type IIAPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktras ProteinsFAKintegrin β1MEK resistanceMLCKmyosin IIA

Identifiers

PMID27563827
PMCPMC5325378
OpenAlexW2511559811

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.