Evidence map›Paper›PMID 36258216›Full record

ArticleWorld journal of surgical oncology2022

CapG promoted nasopharyngeal carcinoma cell motility involving Rho motility pathway independent of ROCK.

Ying Fu, Xiuzhi Zhang, Xujun Liang, Yongheng Chen, Zhuchu Chen, Zhefeng Xiao

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

Article in World journal of surgical oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

8 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Intestinal injury signaling pathway in sepsis.Frontiers in immunology · 2025
    Review
  7. Article
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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.

Ying Fu *Department of Pathology, NHC Key Laboratory of Cancer Proteomics, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Xiuzhi Zhang *Department of Pathology, Henan Medical College, Zhengzhou, 451191, Henan, China.
Xujun LiangDepartment of Pathology, NHC Key Laboratory of Cancer Proteomics, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Yongheng ChenDepartment of Pathology, NHC Key Laboratory of Cancer Proteomics, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Zhuchu ChenDepartment of Pathology, NHC Key Laboratory of Cancer Proteomics, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Zhefeng XiaoDepartment of Pathology, NHC Key Laboratory of Cancer Proteomics, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China. xiaozf@csu.edu.cn.
Xiangya Hospital Central South University · CNCentral South University · CN

Funding

National Natural Science Foundation of China 81202129
6 · The paper itself

Abstract

backgroundGelsolin-like capping actin protein (CapG) modulates actin dynamics and actin-based motility with a debatable role in tumorigenic progression. The motility-associated functions and potential molecular mechanisms of CapG in nasopharyngeal carcinoma (NPC) remain unclear.

methodsCapG expression was detected by immunohistochemistry in a cohort of NPC tissue specimens and by Western blotting assay in a variety of NPC cell lines. Loss of function and gain of function of CapG in scratch wound-healing and transwell assays were performed. Inactivation of Rac1 and ROCK with the specific small molecular inhibitors was applied to evaluate CapG's role in NPC cell motility. GTP-bound Rac1 and phosphorylated-myosin light chain 2 (p-MLC2) were measured in the ectopic CapG overexpressing cells. Finally, CapG-related gene set enrichment analysis was conducted to figure out the significant CapG-associated pathways in NPC.

resultsCapG disclosed increased level in the poorly differentiated NPC tissues and highly metastatic cells. Knockdown of CapG reduced NPC cell migration and invasion in vitro, while ectopic CapG overexpression showed the opposite effect. Ectopic overexpression of CapG compensated for the cell motility loss caused by simultaneous inactivation of ROCK and Rac1 or inactivation of ROCK alone. GTP-bound Rac1 weakened, and p-MLC2 increased in the CapG overexpressing cells. Bioinformatics analysis validated a positive correlation of CapG with Rho motility signaling, while Rac1 motility pathway showed no significant relationship.

conclusionsThe present findings highlight the contribution of CapG to NPC cell motility independent of ROCK and Rac1. CapG promotes NPC cell motility at least partly through MLC2 phosphorylation and contradicts with Rac1 activation.

Indexed as

ActinsNasopharyngeal NeoplasmsCell Line, TumorCell MovementGelsolinGene Expression Regulation, NeoplasticGuanosine TriphosphateHumansMicrofilament ProteinsNasopharyngeal CarcinomaNuclear ProteinsActinsCAPG protein, humanGelsolinGuanosine TriphosphateMicrofilament ProteinsNuclear ProteinsCapGMotilityNasopharyngeal carcinomaRac1ROCK

Identifiers

PMID36258216
PMCPMC9580211
OpenAlexW4306742386

What Socratic holds

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LicenceCC BY
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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.