Evidence map›Paper›PMID 29106388›Full record

ArticleOncogene2018

Calcium signalling links MYC to NUAK1.

T Monteverde, J Tait-Mulder, A Hedley, J R Knight, O J Sansom, D J Murphy

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.3field-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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. NUAK: never underestimate a kinase.Essays in biochemistry · 2024
    Review
  5. LKB1 biology: assessing the therapeutic relevancy of LKB1 inhibitors.Cell communication and signaling : CCS · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Role of ARK5 in cancer and other diseases (Review).Experimental and therapeutic medicine · 2021
    Review
  15. AMPKα-like proteins as LKB1 downstream targets in cell physiology and cancer.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

6 authors at 2 institutions in 1 country.

T MonteverdeInstitute of Cancer Sciences, University of Glasgow, Glasgow, Scotland, UK.
J Tait-MulderInstitute of Cancer Sciences, University of Glasgow, Glasgow, Scotland, UK.
A HedleyCRUK Beatson Institute, Garscube Estate, Glasgow, UK.
J R KnightCRUK Beatson Institute, Garscube Estate, Glasgow, UK.
O J SansomInstitute of Cancer Sciences, University of Glasgow, Glasgow, Scotland, UK.
D J MurphyInstitute of Cancer Sciences, University of Glasgow, Glasgow, Scotland, UK.
Cancer Research UK Scotland Institute · GBUniversity of Glasgow · GB

Funding

Cancer Research UK 21139Wellcome Trust 105614
6 · The paper itself

Abstract

NUAK1 is a member of the AMPK-related family of kinases. Recent evidence suggests that NUAK1 is an important regulator of cell adhesion and migration, cellular and organismal metabolism, and regulation of TAU stability. As such, NUAK1 may play key roles in multiple diseases ranging from neurodegeneration to diabetes and metastatic cancer. Previous work revealed a crucial role for NUAK1 in supporting viability of tumour cells specifically when MYC is overexpressed. This role is surprising, given that NUAK1 is activated by the tumour suppressor LKB1. Here we show that, in tumour cells lacking LKB1, NUAK1 activity is maintained by an alternative pathway involving calcium-dependent activation of PKCα. Calcium/PKCα-dependent activation of NUAK1 supports engagement of the AMPK-TORC1 metabolic checkpoint, thereby protecting tumour cells from MYC-driven cell death, and indeed, MYC selects for this pathway in part via transcriptional regulation of PKCα and ITPR. Our data point to a novel role for calcium in supporting tumour cell viability and clarify the synthetic lethal interaction between NUAK1 and MYC.

Indexed as

Gene Expression Regulation, NeoplasticAMP-Activated Protein KinasesApoptosisBiomarkers, TumorBone NeoplasmsCalciumCalcium SignalingCell ProliferationHeLa CellsHumansOsteosarcomaPhosphorylationProtein Kinase C-alphaProtein KinasesProto-Oncogene Proteins c-mycRepressor ProteinsAMP-Activated Protein KinasesBiomarkers, TumorCalciumMYC protein, humanNUAK1 protein, humanPRKAA1 protein, humanPRKCA protein, humanProtein Kinase C-alphaProtein KinasesProto-Oncogene Proteins c-mycRepressor Proteins

Identifiers

PMID29106388
PMCPMC5815498
OpenAlexW2767541101

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.