Evidence map›Paper›PMID 38217587›Full record

ArticleCancer biomarkers : section A of Disease markers2024

KLF5 inhibits the migration and invasion in cervical cancer cell lines by regulating SNAI1.

Xinjian Qu, Chang Xu, Wenbo Yang, Qianqian Li, Simei Tu, Chenghai Gao

Open access · bronzeAbstract read
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Article in Cancer biomarkers : section A of Disease markers, 2024. 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
0.5field-weighted citation impact, top 39% of its field
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Xinjian QuInstitute of Marine Drugs, Guangxi University of Chinese Medicine, Nanning, Guangxi, China.
Chang XuInstitute of Marine Drugs, Guangxi University of Chinese Medicine, Nanning, Guangxi, China.
Wenbo YangSchool of Life and Pharmaceutical Sciences, Dalian University of Technology, Dalian, Liaoning, China.
Qianqian LiSchool of Life and Pharmaceutical Sciences, Dalian University of Technology, Dalian, Liaoning, China.
Simei TuSchool of Life and Pharmaceutical Sciences, Dalian University of Technology, Dalian, Liaoning, China.
Chenghai GaoInstitute of Marine Drugs, Guangxi University of Chinese Medicine, Nanning, Guangxi, China.
Dalian University of Technology · CNGuangxi University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpithelial-mesenchymal transition (EMT) is an important biological process by which malignant tumor cells to acquire migration and invasion abilities. This study explored the role of KLF5 in the EMT process of in cervical cancer cell lines.

objectiveKrüpple-like factor 5 (KLF5) is a basic transcriptional factor that plays a key role in cell-cycle arrest and inhibition of apoptosis. However, the molecular mechanism by which KLF5 mediates the biological functions of cervical cancer cell lines has not been elucidated. Here, we focus on the potential function of ELF5 in regulating the EMT process in in vitro model of cervical cancer cell lines.

methodWestern-blot and real-time quantitative PCR were used to detect the expression of EMT-related genes in HeLa cells. MTT assays, cell scratch and Transwell assays were used to assess HeLa cells proliferation and invasion capability. Using the bioinformatics tool JASPAR, we identified a high-scoring KLF5-like binding sequence in the SNAI1 gene promoter. Luciferase reporter assays was used to detect transcriptional activity for different SNAI1 promoter truncates.

resultAfter overexpressing the KLF5 gene in HeLa cells, KLF5 not only significantly inhibited the invasion and migration of HeLa cells, but also increased the expression of E-cadherin and decreased the expression of N-cadherin and MMP9. In addition, the mRNA expression of upstream regulators of E-cadherin, such as SNAI1, SLUG, ZEB1/2 and TWIST1 was also decreased. Furthermore, KLF5 inhibiting the expression of the SNAI1 gene via binding its promoter region, and the EMT of Hela cells was promoted after overexpression of the SNAI1 gene.

conclusionThese results indicate that KLF5 can downregulate the EMT process of HeLa cells by decreasing the expression of the SNAI1 gene, thereby inhibiting the migration and invasion of HeLa cervical cancer cells.

Indexed as

Uterine Cervical NeoplasmsCadherinsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFactor VFemaleGene Expression Regulation, NeoplasticHeLa CellsHumansKruppel-Like Transcription FactorsSnail Family Transcription FactorsCadherinsFactor VKLF5 protein, humanKruppel-Like Transcription FactorsSNAI1 protein, humanSnail Family Transcription Factorscervical cancer cellsEMTKLF5SNAI1

Identifiers

PMID38217587
PMCPMC11191462
OpenAlexW4390747790

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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.