Evidence map›Paper›PMID 38001389›Full record

ArticleBiochemical genetics2024

Cellular Retinoic Acid Binding Protein 2 (CRABP2), Up-regulated by HPV E6/E7, Leads to Aberrant Activation of the Integrin β1/FAK/ERK Signaling Pathway and Aggravates the Malignant Phenotypes of Cervical Cancer.

Jiaxin Liu, Lu Tang, Wenzhu Chu, Lanlan Wei

Abstract read
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In one paragraph

Article in Biochemical genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Jiaxin LiuSchool of Medical Technology, Taizhou Polytechnic College, Taizhou, Jiangsu, 225300, China.
Lu TangHarbin Medical University, Immunity and Infection, Pathogenic Biology Key Laboratory, Heilongjiang, 150081, China.
Wenzhu ChuDepartment of Dermatology, Hongqi Hospital, Mudanjiang Medical University, Heilongjiang, 157001, China.
Lanlan WeiNational Clinical Research Center for Infectious Diseases; Institute for Hepatology, The Third People's Hospital of Shenzhen; The Second Hospital Affiliated to Southern University of Science and Technology, Shenzhen, Guangdong, 518000, China. weilanlan@mail.sustech.edu.cn.
Harbin Medical University · CNMudanjiang Medical University · CN

Funding

Natural Science Foundation of China 82102822Shenzhen Longgang Fund for Science and Technology Project LGKCYLWS2020101Shenzhen Science and Technology R&D Fund JCYJ20210324131607019
6 · The paper itself

Abstract

The ectopic expression of cellular retinoic acid binding protein 2 (CRABP2) is associated with various tumorigenesis. However, the effects of CRABP2 on the progression of cervical cancer are still unclear. The current study aimed to investigate the role of CRABP2 in the malignant phenotypes of cervical cancer cells. CRABP2 was artificially regulated in CaSki, SiHa, and C-33A cells. CCK-8 assay and flow cytometry were used to assess the cell proliferation and apoptosis abilities, respectively. Wound healing assay and transwell assay were employed to measure the cell migration and invasion abilities, respectively. The results showed that CRABP2 was highly expressed in cervical carcinoma tissues and cell lines, and its high expression was associated with poor overall survival. Knockdown of CRABP2 promoted the cell apoptosis and inhibited cell proliferation, migration, and invasion in cervical carcinoma cells, whereas CRABP2 overexpression exhibited the opposite results. Mechanically, CRABP2 silencing suppressed the Integrin β1/FAK/ERK signaling via HuR. Treatment with siITGB1 or a FAK inhibitor PF-562271 or an ERK inhibitor FR180204 reversed the promoting effects of CRABP2 on cell proliferation, migration, and invasion. Moreover, the overexpression of CRABP2 reverted the HPV16 E6/E7 knockdown-induced inhibition of cell proliferation, migration, and invasion in cervical cancer cells. These results suggested that HPV16 E6/E7 promoted the malignant phenotypes of cervical cancer by upregulating the expression of CRABP2. In conclusion, CRABP2, upregulated by HPV E6/E7, promoted the progression of cervical cancer through activating the Integrin β1/FAK/ERK signaling pathway via HuR.

Indexed as

Focal Adhesion Kinase 1Integrin beta1MAP Kinase Signaling SystemOncogene Proteins, ViralReceptors, Retinoic AcidUp-RegulationUterine Cervical NeoplasmsCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansPapillomavirus E7 ProteinsPhenotypeRepressor ProteinsE6 protein, Human papillomavirus type 16Focal Adhesion Kinase 1Integrin beta1Itgb1 protein, humanoncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 ProteinsPTK2 protein, humanReceptors, Retinoic AcidRepressor Proteinsretinoic acid binding protein II, cellularCellular retinoic acid binding protein 2Cervical carcinomaHPV16 E6/E7Integrin β1/FAK/ERK signaling

Identifiers

PMID38001389
OpenAlexW4388967629

What OpenQuestion holds

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Registered trials

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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.