Evidence map›Paper›PMID 38975937›Full record

ArticleAging2024

LIMK1 promotes the development of cervical cancer by up-regulating the ROS/Src-FAK/cofilin signaling pathway.

Yajing Jia, Yongping Li, Naiyi Du, Wei Zhao, Yakun Liu

Abstract read
In one paragraph

Article in Aging, 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
–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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. [Therapeutic mechanism of hederagenin, an active component inNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    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

5 authors.

Yajing JiaDepartment of Gynecology, The Fourth Hospital of Hebei Medical University, Shijiazhuang, P.R. China.
Yongping LiDepartment of Gynecology, The Fourth Hospital of Hebei Medical University, Shijiazhuang, P.R. China.
Naiyi DuDepartment of Gynecology, The Fourth Hospital of Hebei Medical University, Shijiazhuang, P.R. China.
Wei ZhaoDepartment of Gynecology, The Fourth Hospital of Hebei Medical University, Shijiazhuang, P.R. China.
Yakun LiuDepartment of Gynecology, The Fourth Hospital of Hebei Medical University, Shijiazhuang, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveIn this study, we investigated the mechanism of action of LIMK1 in cervical cancer progression.

methodsThe biological role of LIMK1 in regulating the growth, invasion, and metastasis of cervical cancer was studied in SiHa, CaSki cells and nude mice tumor models. The role of LIMK1 in the growth of cervical cancer was evaluated by HE staining. The role of LIMK1 in the invasion, metastasis, and proliferation of cervical cancer was evaluated by cell scratch, Transwell, and monoclonal experiments. The interaction among LIMK1, ROS, and Src was evaluated by Western blotting. The effects of regulating ROS and p-Src expression on LIMK1 in the migration/invasion and proliferation of cervical cancer cells were evaluated through cellular functional assays.

resultsOverexpression of LIMK1 promoted tumor growth in nude mice. Cell scratch, Transwell, and monoclonal experiments suggested that LIMK1 promoted the invasion, metastasis, and proliferation of cervical cancer cells. Western blotting suggested that LIMK1 can promote the expression of ROS-related proteins NOX2, NOX4, p-Src, and downstream proteins p-FAK, p-ROCK1/2, p-Cofilin-1, F-actin and inhibit the expression of p-SHP2 protein. Correction experiments showed that LIMK1 regulated the expression of p-FAK and p-Cofilin-1 proteins by regulating ROS and p-Src. Through the detection of cervical cancer cell functions, it was found that the activation of ROS and p-Src induced by LIMK1 is an early event that promotes the migration, proliferation, and invasion of cervical cancer cells.

conclusionsLIMK1 promotes the expression of F-actin and promotes the development of cervical cancer by regulating the oxidative stress/Src-mediated p-FAK/p-ROCK1/2/p-Cofilin-1 pathway.

Indexed as

Lim KinasesMice, NudeReactive Oxygen SpeciesSignal TransductionUterine Cervical NeoplasmsActin Depolymerizing FactorsAnimalsCell Line, TumorCell MovementCell ProliferationCofilin 1FemaleFocal Adhesion Kinase 1Gene Expression Regulation, NeoplasticHumansMiceActin Depolymerizing FactorsCofilin 1Focal Adhesion Kinase 1LIMK1 protein, humanLim KinasesPTK2 protein, humanReactive Oxygen Speciessrc-Family Kinasescervical cancerLIMK1oxidative stressSrc

Identifiers

PMID38975937
PMCPMC11272116

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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.