Evidence map›Paper›PMID 36694148›Full record

ArticleBMC cancer2023

C/EBPβ expression decreases in cervical cancer and leads to tumorigenesis.

Haichen Long, Yangyang Li, Huijuan Wang, Bingxuan Guo, Shuyan Song, Xiangyi Zhe, Hongtao Li, Dongmei Li, Renfu Shao, Zemin Pan

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

Article in BMC cancer, 2023. 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
1.1field-weighted citation impact, top 23% 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, 7 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

10 authors at 2 institutions in 2 countries.

Haichen Long *Department of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, 832002, Xinjiang, China.
Yangyang Li *Department of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, 832002, Xinjiang, China.
Huijuan Wang *Department of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, 832002, Xinjiang, China.
Bingxuan GuoDepartment of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, 832002, Xinjiang, China.
Shuyan SongDepartment of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, 832002, Xinjiang, China.
Xiangyi ZheDepartment of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, 832002, Xinjiang, China. 342480821@qq.com.
Hongtao LiDepartment of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, 832002, Xinjiang, China.
Dongmei LiDepartment of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, 832002, Xinjiang, China.
Renfu ShaoCentre for Bioinnovation, School of Science, Technology and Engineering, University of the Sunshine Coast, Maroochydore, 4556, Australia.
Zemin PanDepartment of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, 832002, Xinjiang, China. 1764026209@qq.com.
Shihezi University · CNUniversity of the Sunshine Coast · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCervical cancer is currently estimated to be the fourth most common cancer among women worldwide and the leading cause of cancer-related deaths in some of the world's poorest countries. C/EBPβ has tumor suppressor effects because it is necessary for oncogene-induced senescence. However, C/EBPβ also has an oncogenic role. The specific role of C/EBPβ in cervical cancer as a tumor suppressor or oncoprotein is unclear.

objectiveTo explore the role of the C/EBPβ protein in cervical tumorigenesis and progression.

methodsQuantitative RT-PCR was used to analyze C/EBPβ (15 cervical cancer tissue samples and 15 corresponding normal cervical tissue samples), miR-661, and MTA1 mRNA expression in clinical samples (10 cervical cancer tissue samples and 10 corresponding normal cervical tissue samples). Immunohistochemistry was used to analyze C/EBPβ (381 clinical samples), Ki67 (80 clinical samples) and PCNA ( 60 clinical samples) protein expression. MALDI-TOF MassARRAY was used to analyze C/EBPβ gene methylation (13 cervical cancer tissues and 13 corresponding normal cervical tissues). Cell proliferation was analyzed by CCK-8 in cervical cancer cell lines. Western blotting and immunohistochemistry were performed to detect C/EBPβ protein expression levels, and mRNA expression was analyzed by quantitative RT-PCR analysis. Flow cytometry was performed to measure cell cycle distribution and cell apoptosis. Colony formation, Transwell, cell invasion, and wound healing assays were performed to detect cell migration and invasion.

resultsC/EBPβ protein expression was significantly reduced in cervical cancer tissues compared with cervicitis tissues (P < 0.01). Ki67 protein and PCNA protein expression levels were significantly higher in cervical cancer tissues compared with cervicitis tissues. The rate of C/EBPβ gene promoter methylation of CpG12, 13, 14 and CpG19 in cervical cancer tissues was significantly increased compared with normal cervical tissue (P < 0.05). In addition, C/EBPβ was overexpressed in cervical cancer cells and this overexpression inhibited cell proliferation, migration, invasion, arrested cells in S phase, and promoted apoptosis.

conclusionsWe have demonstrated that C/EBPβ decreased in cervical cancer tissues and overexpression of the C/EBPβ gene in cervical cancer cells could inhibit proliferation, invasion and migration.

Indexed as

MicroRNAsUterine Cervical NeoplasmsUterine CervicitisCarcinogenesisCCAAT-Enhancer-Binding Protein-betaCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticFemaleGene Expression Regulation, NeoplasticHumansKi-67 AntigenProliferating Cell Nuclear AntigenRepressor ProteinsRNA, MessengerCCAAT-Enhancer-Binding Protein-betaCEBPB protein, humanKi-67 AntigenMicroRNAsMIRN661 microRNA, humanMTA1 protein, humanPCNA protein, humanProliferating Cell Nuclear AntigenRepressor ProteinsRNA, MessengerTrans-ActivatorsC/EBPβCervical cancerGene expressionInvasionMigrationProliferation

Identifiers

PMID36694148
PMCPMC9872280
OpenAlexW4317820225

What OpenQuestion holds

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LicenceCC BY
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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.