Evidence map›Paper›PMID 38419282›Full record

ArticleMolecular oncology2024

The CK1ε/SIAH1 axis regulates AXIN1 stability in colorectal cancer cells.

Mengfang Yan, Zijie Su, Xiaoyi Pang, Hanbin Wang, Han Dai, Jiong Ning, Shanshan Liu, Qi Sun, Jiaxing Song, Xibao Zhao and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 47% 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

3 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
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

11 authors at 3 institutions in 1 country.

Mengfang YanGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, China.
Zijie SuGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, China.
Xiaoyi PangGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, China.
Hanbin WangGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, China.
Han DaiGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, China.
Jiong NingGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, China.
Shanshan LiuGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, China.
Qi SunGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, China.
Jiaxing SongGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, China.
Xibao ZhaoGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, China.ORCID 0000-0002-8708-9567
Desheng LuGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, China.ORCID 0000-0002-0314-5649
Shenzhen University Health Science Center · CNShenzhen University · CNGuangxi Medical University · CN

Funding

National Natural Science Foundation of China 31900881National Natural Science Foundation of China 31970739National Natural Science Foundation of China 32100700National Natural Science Foundation of China 81802662National Natural Science Foundation of China 82273485National Natural Science Foundation of China U21A20421Natural Science Foundation of Guangdong Province 2020A1515010340Natural Science Foundation of Guangdong Province 2020A1515010543Natural Science Foundation of Guangdong Province 2021A1515011164Natural Science Foundation of Guangdong Province 2022A1515010598Shenzhen Key Basic Research Program JCYJ20200109105001821Shenzhen Science and Technology Innovation Program JCYJ20210324094405014Stable Support Project of Shenzhen 20200826134656001Stable Support Project of Shenzhen 20231120113237002
6 · The paper itself

Abstract

Casein kinase 1ε (CK1ε) and axis inhibitor 1 (AXIN1) are crucial components of the β-catenin destruction complex in canonical Wnt signaling. CK1ε has been shown to interact with AXIN1, but its physiological function and role in tumorigenesis remain unknown. In this study, we found that CK1δ/ε inhibitors significantly enhanced AXIN1 protein level in colorectal cancer (CRC) cells through targeting CK1ε. Mechanistically, CK1ε promoted AXIN1 degradation by the ubiquitin-proteasome pathway by promoting the interaction of E3 ubiquitin-protein ligase SIAH1 with AXIN1. Genetic or pharmacological inhibition of CK1ε and knockdown of SIAH1 downregulated the expression of Wnt/β-catenin-dependent genes, suppressed the viability of CRC cells, and restrained tumorigenesis and progression of CRC in vitro and in vivo. In summary, our results demonstrate that CK1ε exerted its oncogenic role in CRC occurrence and progression by regulating the stability of AXIN1. These findings reveal a novel mechanism by which CK1ε regulates the Wnt/β-catenin signaling pathway and highlight the therapeutic potential of targeting the CK1ε/SIAH1 axis in CRC.

Indexed as

Axin ProteinCasein Kinase 1 epsilonColorectal NeoplasmsUbiquitin-Protein LigasesWnt Signaling PathwayAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB CMice, NudeNuclear ProteinsProtein StabilitySeven in Absentia ProteinsAXIN1 protein, humanAxin ProteinCasein Kinase 1 epsilonNuclear ProteinsSeven in Absentia ProteinsUbiquitin-Protein LigasesAXIN1CK1εcolorectal cancerSIAH1ubiquitinationWnt/β‐catenin

Identifiers

PMID38419282
PMCPMC11467792
OpenAlexW4392289514

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.