Evidence map›Paper›PMID 38185060›Full record

ArticleTranslational oncology2024

CK1δ/ε inhibition induces ULK1-mediated autophagy in tumorigenesis.

Vivian Weiwen Xue, Shanshan Liu, Qi Sun, Jiong Ning, Huan Li, Weilan Wang, Sapna Sayed, Xibao Zhao, Li Fu, Desheng Lu

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

Article in Translational oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 42% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

10 authors at 2 institutions in 3 countries.

Vivian Weiwen XueDepartment of Pharmacology, Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Marshall Laboratory of Biomedical Engineering, Shenzhen University Health Science Center, No. 1066 Xueyuan Avenue, Nanshan District, Shenzhen 518060, China; College of Health Science and Environmental Engineering, Shenzhen Technology University, Shenzhen, China.
Shanshan LiuDepartment of Pharmacology, Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Marshall Laboratory of Biomedical Engineering, Shenzhen University Health Science Center, No. 1066 Xueyuan Avenue, Nanshan District, Shenzhen 518060, China.
Qi SunDepartment of Pharmacology, Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Marshall Laboratory of Biomedical Engineering, Shenzhen University Health Science Center, No. 1066 Xueyuan Avenue, Nanshan District, Shenzhen 518060, China.
Jiong NingDepartment of Pharmacology, Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Marshall Laboratory of Biomedical Engineering, Shenzhen University Health Science Center, No. 1066 Xueyuan Avenue, Nanshan District, Shenzhen 518060, China; Center for Molecular Biomedicine, Friedrich-Schiller-Universität Jena, Jena, Germany.
Huan LiDepartment of Pharmacology, Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Marshall Laboratory of Biomedical Engineering, Shenzhen University Health Science Center, No. 1066 Xueyuan Avenue, Nanshan District, Shenzhen 518060, China.
Weilan WangCenter for Healthy Longevity, National University of Singapore, Singapore.
Sapna SayedDepartment of Pharmacology, Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Marshall Laboratory of Biomedical Engineering, Shenzhen University Health Science Center, No. 1066 Xueyuan Avenue, Nanshan District, Shenzhen 518060, China.
Xibao ZhaoDepartment of Pharmacology, Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Marshall Laboratory of Biomedical Engineering, Shenzhen University Health Science Center, No. 1066 Xueyuan Avenue, Nanshan District, Shenzhen 518060, China.
Li FuDepartment of Pharmacology, Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Marshall Laboratory of Biomedical Engineering, Shenzhen University Health Science Center, No. 1066 Xueyuan Avenue, Nanshan District, Shenzhen 518060, China. Electronic address: gracelfu@szu.edu.cn.
Desheng LuDepartment of Pharmacology, Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Marshall Laboratory of Biomedical Engineering, Shenzhen University Health Science Center, No. 1066 Xueyuan Avenue, Nanshan District, Shenzhen 518060, China. Electronic address: delu@szu.edu.cn.
Shenzhen University Health Science Center · CNNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAutophagy is an important mechanism of cell homeostasis maintenance. As essential serine/threonine-protein kinases, casein kinase I family members affect tumorigenesis by regulating a variety of cellular progression. However, the mechanism by which they regulate autophagy remains unclear. MATERIALS AND

methodsWe silenced CK1δ/ε in cancer cells and observed cell morphology, the expression of autophagy-related genes, and its impact on cancer cell growth and viability. By inhibiting CK1δ/ε-induced upregulation of autophagy genes, we profiled the regulatory mechanism of CK1δ/ε on autophagy and cancer cell growth. The impact of CK1δ/ε inhibition on tumor cell growth was also assessed in vivo.

resultsHere, we found that CK1δ/ε played an important role in ULK1-mediated autophagy regulation in both lung cancer and melanoma cells. Mechanically, silencing CK1δ/ε increased ULK1 expression with enhanced autophagic flux and suppressed cancer cell proliferation, while ULK1 knockdown blocked the activation of autophagy caused by CK1δ/ε inhibition. By silencing CK1δ/ε in syngeneic mouse model bearing LLC1 murine lung cancer cells in vivo, we observed tumor growth suppression mediated by CK1δ/ε inhibition.

conclusionOur results provide evidence for the role of CK1δ/ε in the regulation of tumorigenesis via the ULK1-mediated autophagy, and also suggest the impact of CK1δ/ε inhibition on tumor growth and its significance as a potential therapeutic target.

Indexed as

AutophagyCK1δ/εTumorigenesisULK1

Identifiers

PMID38185060
PMCPMC10808987
OpenAlexW4390645235

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.