Evidence map›Paper›PMID 40566856›Full record

ArticleCell adhesion & migration2025

Loss of CDS1 impairs the tumorigenic characteristics of nasopharyngeal carcinoma by modulating lipid metabolism.

Yifang Wang, Limei Li, Liudmila Matskova, Lixian Deng, Danping Li, Yi Huang, Haili Liang, Wen Wang, Ziyuan Liang, Jiaming Su and 6 more

Abstract read
In one paragraph

Article in Cell adhesion & migration, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Yifang WangMinistry of Education, Key Laboratory of High-Incidence-Tumor Prevention & Treatment (Guangxi Medical University), Nanning, China.
Limei LiMinistry of Education, Key Laboratory of High-Incidence-Tumor Prevention & Treatment (Guangxi Medical University), Nanning, China.
Liudmila MatskovaInstitute of Molecular Biology and Biophysics, Federal Research Center of Fundamental and Translational Medicine (IMBB FRC FTM), Novosibirsk, Russia.
Lixian DengMinistry of Education, Key Laboratory of High-Incidence-Tumor Prevention & Treatment (Guangxi Medical University), Nanning, China.
Danping LiMinistry of Education, Key Laboratory of High-Incidence-Tumor Prevention & Treatment (Guangxi Medical University), Nanning, China.
Yi HuangDepartment of Otolaryngology-Head and Neck Surgery, First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Haili LiangGuangxi Zhuang Autonomous Region Institute of Product Quality Inspection, Nanning, China.
Wen WangGuangxi Zhuang Autonomous Region Institute of Product Quality Inspection, Nanning, China.
Ziyuan LiangMinistry of Education, Key Laboratory of High-Incidence-Tumor Prevention & Treatment (Guangxi Medical University), Nanning, China.
Jiaming SuGuangxi Zhuang Autonomous Region Institute of Product Quality Inspection, Nanning, China.
Weilin ZhaoGuangxi Zhuang Autonomous Region Institute of Product Quality Inspection, Nanning, China.
Tingting HuangMinistry of Education, Key Laboratory of High-Incidence-Tumor Prevention & Treatment (Guangxi Medical University), Nanning, China.
Jiemei ChuLife Science Institute, Guangxi Medical University, Nanning, China.
Zhe ZhangGuangxi Zhuang Autonomous Region Institute of Product Quality Inspection, Nanning, China.
Xue XiaoGuangxi Zhuang Autonomous Region Institute of Product Quality Inspection, Nanning, China.
Xiaoying ZhouMinistry of Education, Key Laboratory of High-Incidence-Tumor Prevention & Treatment (Guangxi Medical University), Nanning, China.ORCID 0000-0003-3298-5089

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The accumulation of lipid droplets (LDs) enhancing nasopharyngeal carcinoma (NPC) cell migration. We reveals that CDP-diacylglycerol synthase 1 (CDS1), an inhibitor of LDs formation, is significantly downregulated in NPC. Restoring CDS1 expression suppresses NPC cell growth, colony formation, tumorigenesis, migration, and invasion. The anti-cancer effect of CDS1 is attributed to its role in decreasing the intracellular LDs. Moreover, CDS1 promotes activation of the NF-κB signaling pathway, resulting in elevated levels of inflammatory cytokines within NPC cells. This is likely to enhance the immunogenicity of these cells, thereby reducing tumor volume in the in vivo model. These findings establish CDS1 as a novel suppressor of NPC by modulating LDs levels, suggesting potential therapeutic avenues aimed at limiting LDs accumulation.

Indexed as

CarcinogenesisLipid MetabolismNasopharyngeal CarcinomaNasopharyngeal NeoplasmsAnimalsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansLipid DropletsMiceMice, NudeNeoplasm InvasivenessNF-kappa BSignal TransductionNF-kappa BCDP-diacylglycerol synthase 1inflammatory cytokineslipid dropletsNasopharyngeal carcinomaNF-κB signaling pathway

Identifiers

PMID40566856
PMCPMC12203838

What Socratic 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 Socratic graph.