Evidence map›Paper›PMID 37094736›Full record

ReviewCancer letters2023

The mammalian Sterile 20-like kinase 4 (MST4) signaling in tumor progression: Implications for therapy.

Ayechew A Getu, Ming Zhou, Shi-Yuan Cheng, Ming Tan

Open access · hybridAbstract readReview
In one paragraph

Review in Cancer letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
5.0field-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

10 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. MST4 as a key driver of osteoclast activation in osteoporosis.Journal of pharmaceutical analysis · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Autophagy and cancer therapy.Cancer letters · 2024
    Review
  10. 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

4 authors at 3 institutions in 4 countries.

Ayechew A GetuGraduate Institute of Biomedical Sciences, China Medical University, Taichung, 406040, Taiwan; Department of Physiology, School of Medicine, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia.
Ming ZhouCancer Research Institute and School of Basic Medical Sciences, Central South University, Changsha, China.
Shi-Yuan ChengThe Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute at Northwestern Medicine, The Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, USA.
Ming TanGraduate Institute of Biomedical Sciences, China Medical University, Taichung, 406040, Taiwan; Institute of Biochemistry & Molecular Biology, China Medical University, Taichung, 406040, Taiwan. Electronic address: mingtan@mail.cmu.edu.tw.
China Medical University · TWCentral South University · CNNorthwestern University · US

Funding

Targeting RNA Splicing in GliomaR01NS125318 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Shi-Yuan Cheng · 2022 to 2026
$2.4M
Role of Protein Methylation in Cell Mitosis and GlioblastomaR01NS115403 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CHENG, SHI-YUAN · 2020 to 2024
$2.1M
Cysteine Depletion-induced Ferroptosis as a Therapeutic Vulnerability iR21NS126810 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CHENG, SHI-YUAN · 2022 to 2023
$440k
Targeting ATG4B to Treat GlioblastomaR21NS122375 · NINDS · NORTHWESTERN UNIVERSITY · PI CHENG, SHI-YUAN, SCHEIDT, KARL A · 2022 to 2023
$423k
Identification of Long Non-coding RNAs as Novel Biomarkers for Heterogeneous GlioblastomasR21CA209345 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CHENG, SHI-YUAN, ZHANG, WEI · 2016 to 2017
$365k
NCI NIH HHS R21 CA209345NINDS NIH HHS R01 NS115403NINDS NIH HHS R01 NS125318NINDS NIH HHS R21 NS122375
6 · The paper itself

Abstract

Cancer is a leading cause of death in humans, with a complex and dynamic nature that makes it challenging to fully comprehend and treat. The Mammalian Sterile 20-Like Kinase 4 (MST4 or STK26) is a serine/threonine-protein kinase that plays a crucial role in cell migration and polarity in both normal and tumor cells via activation of intracellular signaling molecules and pathways. MST4 is involved in tumor cell proliferation, migration and invasion, epithelial-mesenchymal transition (EMT), survival, and cancer metastasis through modulation of downstream signaling pathways including the extracellular signal-regulated kinase (ERK) and protein kinase B (AKT) pathways. Additionally, MST4 interacts with programmed cell death 10 (PDCD10) to promote tumor proliferation and migration. MST4 phosphorylates autophagy related 4B cysteine peptidase (ATG4B) to mediate autophagy signaling, promote tumor cell survival and proliferation, and contribute to treatment resistance. Taken together, MST4 functions as an oncogene and is a promising therapeutic target which deserves further exploration.

Indexed as

Protein Serine-Threonine KinasesSignal TransductionAnimalsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionExtracellular Signal-Regulated MAP KinasesHippo KinasesHumansMammalsOncogenesProto-Oncogene Proteins c-aktExtracellular Signal-Regulated MAP KinasesHippo KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktSTK26 protein, humanCancerEMTMST4MST kinasesPathways

Identifiers

PMID37094736
PMCPMC10642761
OpenAlexW4366752921

What OpenQuestion holds

Textmetadata
LicenceTDM
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.