Evidence map›Paper›PMID 29166822›Full record

ReviewCell adhesion & migration2018

Myeloid cell leukemia 1 (MCL-1), an unexpected modulator of protein kinase signaling during invasion.

Adelaide Ij Young, Paul Timpson, David Gallego-Ortega, Christopher J Ormandy, Samantha R Oakes

Open access · goldAbstract readReview
In one paragraph

Review in Cell adhesion & migration, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  12. Venetoclax resistance: mechanistic insights and future strategies.Cancer drug resistance (Alhambra, Calif.) · 2022
    Review
  13. Review
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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

5 authors at 1 institution in 1 country.

Adelaide Ij Younga Cancer Research Division , Garvan Institute of Medical Research and the Kinghorn Cancer Centre , 384 Victoria Street, Darlinghurst , NSW , Australia.ORCID 0000-0002-5714-0501
Paul Timpsona Cancer Research Division , Garvan Institute of Medical Research and the Kinghorn Cancer Centre , 384 Victoria Street, Darlinghurst , NSW , Australia.ORCID 0000-0002-5514-7080
David Gallego-Ortegaa Cancer Research Division , Garvan Institute of Medical Research and the Kinghorn Cancer Centre , 384 Victoria Street, Darlinghurst , NSW , Australia.ORCID 0000-0002-2347-7835
Christopher J Ormandya Cancer Research Division , Garvan Institute of Medical Research and the Kinghorn Cancer Centre , 384 Victoria Street, Darlinghurst , NSW , Australia.ORCID 0000-0002-2504-7919
Samantha R Oakesa Cancer Research Division , Garvan Institute of Medical Research and the Kinghorn Cancer Centre , 384 Victoria Street, Darlinghurst , NSW , Australia.ORCID 0000-0003-1838-2310
Garvan Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloid cell leukemia-1 (MCL-1), closely related to B-cell lymphoma 2 (BCL-2), has a well-established role in cell survival and has emerged as an important target for cancer therapeutics. We have demonstrated that inhibiting MCL-1 is efficacious in suppressing tumour progression in pre-clinical models of breast cancer and revealed that in addition to its role in cell survival, MCL-1 modulated cellular invasion. Utilizing a MCL-1-specific genetic antagonist, we found two possible mechanisms; firstly MCL-1 directly binds to and alters the phosphorylation of the cytoskeletal remodeling protein, Cofilin, a protein important for cytoskeletal remodeling during invasion, and secondly MCL-1 modulates the levels SRC family kinases (SFKs) and their targets. These data provide evidence that MCL-1 activities are not limited to endpoints of extracellular and intracellular signaling culminating in cell survival as previously thought, but can directly modulate the output of SRC family kinases signaling during cellular invasion. Here we review the pleotropic roles of MCL-1 and discuss the implications of this newly discovered effect on protein kinase signaling for the development of cancer therapeutics.

Indexed as

AnimalsBreast NeoplasmsCell SurvivalHumansMyeloid Cell Leukemia Sequence 1 ProteinMyeloid CellsProtein KinasesSignal TransductionMyeloid Cell Leukemia Sequence 1 ProteinProtein KinasescancerinvasionmetastasisMyeloid cell leukemia 1protein kinase signalingSRC family kinases

Identifiers

PMID29166822
PMCPMC6363037
OpenAlexW2770736726

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.