Evidence map›Paper›PMID 26622315›Full record

ArticleInfectious agents and cancer2015

miR-23b as a potential tumor suppressor and its regulation by DNA methylation in cervical cancer.

Gabriela Elizabeth Campos-Viguri, Hilda Jiménez-Wences, Oscar Peralta-Zaragoza, Gricenda Torres-Altamirano, Diana Guillermina Soto-Flores, Daniel Hernández-Sotelo, Luz Del Carmen Alarcón-Romero, Marco Antonio Jiménez-López, Berenice Illades-Aguiar, Gloria Fernández-Tilapa

Open access · goldAbstract read
In one paragraph

Article in Infectious agents and cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 45 citations in OpenAlex.

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  14. MicroRNAs and Long Non-coding RNAs in c-Met-Regulated Cancers.Frontiers in cell and developmental biology · 2020
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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 1 country.

Gabriela Elizabeth Campos-ViguriLaboratorio de Investigación Clínica, Unidad Académica de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Av. Lázaro Cárdenas S/N, Ciudad Universitaria, Colonia La Haciendita, C.P. 39089 Chilpancingo, Guerrero México.
Hilda Jiménez-WencesLaboratorio de Investigación Clínica, Unidad Académica de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Av. Lázaro Cárdenas S/N, Ciudad Universitaria, Colonia La Haciendita, C.P. 39089 Chilpancingo, Guerrero México.
Oscar Peralta-ZaragozaInstituto Nacional de Salud Pública, Avenida Universidad No. 655, Colonia, Santa María Ahuacatitlán, Cuernavaca, Morelos C.P. 62100 México.
Gricenda Torres-AltamiranoLaboratorio de Investigación Clínica, Unidad Académica de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Av. Lázaro Cárdenas S/N, Ciudad Universitaria, Colonia La Haciendita, C.P. 39089 Chilpancingo, Guerrero México.
Diana Guillermina Soto-FloresLaboratorio de Investigación Clínica, Unidad Académica de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Av. Lázaro Cárdenas S/N, Ciudad Universitaria, Colonia La Haciendita, C.P. 39089 Chilpancingo, Guerrero México.
Daniel Hernández-SoteloLaboratorio de Virología y Epigenética del Cáncer, Unidad Académica de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Av. Lázaro Cárdenas S/N, Ciudad Universitaria, Colonia La Haciendita, C.P. 39089 Chilpancingo, Guerrero México.
Luz Del Carmen Alarcón-RomeroLaboratorio de Investigación en Citopatología e Histoquímica, Unidad Académica de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Av. Lázaro Cárdenas S/N, Ciudad Universitaria, Colonia La Haciendita, C.P. 39089 Chilpancingo, Guerrero México.
Marco Antonio Jiménez-LópezInstituto Estatal de Cancerología "Dr. Arturo Beltrán Ortega", Av. Adolfo Ruiz Cortines No. 128-A, Colonia Alta Progreso, Acapulco de Juárez, Guerrero C.P. 39570 México.
Berenice Illades-AguiarLaboratorio de Biomedicina Molecular, Unidad Académica de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Av. Lázaro Cárdenas S/N, Ciudad Universitaria, Colonia La Haciendita, Chilpancingo, Guerrero C.P. 39089 México.
Gloria Fernández-TilapaLaboratorio de Investigación Clínica, Unidad Académica de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Av. Lázaro Cárdenas S/N, Ciudad Universitaria, Colonia La Haciendita, C.P. 39089 Chilpancingo, Guerrero México.
Universidad Autónoma de Guerrero · MXInstituto Nacional de Salud Pública · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe aberrant expression of miR-23b is involved in the development and progression of cancer. The aim of this study was to evaluate the potential role of methylation in the silencing of miR-23b in cervical cancer cell lines and to determine its expression in stages of malignant progression and in cervical cancer tissues HPV16-positive.

methodsThe methylation of the miR-23b promoter was determined in HeLa, SiHa, CaSki and C33A cells using a Human Cancer miRNA EpiTectMethyl II Signature PCR Array®. The cells were treated with 5-Aza-2'-deoxycytidine, and the expression of miR-23b, uPa, c-Met and Zeb1 was determined by qRT-PCR. miR-92a and GAPDH were used as controls. The expression of miR-23b was determined in cervical scrapes and biopsies of women without squamous intraepithelial lesions, with precursor lesions and with cervical cancer, all were HPV16-positive. The Fisher exact and Mann-Whitney tests were used to compare the differences of the expression of miR-23b, uPa, c-Met and Zeb1 among cell groups, and the difference among patients, respectively. The association between the expression of miR-23b and cervical cancer was determined by logistic regression with a confidence level of 95 %. A value of p < 0.05 was considered statistically significant.

resultsIn C33A, HeLa and CaSki cells, methylation was associated with decreased expression of miR-23b. After treatment with 5-Aza-CdR, the expression of miR-23b increased in all cell lines and the expression of c-Met decreased in HeLa cells, while uPa and Zeb1 decreased in C33A and CaSki cells. In SiHa cells the expression of uPa, c-Met and Zeb1 increased. The expression of miR-23b decreased in relation to the increase in the severity of the lesion and was significantly lower in cervical cancer. In women with premalignant lesions HPV16-positive, decreased levels of miR-23b increased the risk of cervical cancer (OR = 36, 95 % CI = 6.7-192.6, p < 0.05).

conclusionsThe results suggest that the expression of miR-23b is regulated by the methylation of its promoter and is possible that this microRNA influence the expression of uPa, c-Met and Zeb1 in cervical cancer cells lines. In women with premalignant lesions and cervical cancer infected with HPV16, the expression level of miR-23b agree with a tumor suppressor gene.

Indexed as

cervical cancerc-metDNA methylationexpressionHPV16miR-23bupazeb1

Identifiers

PMID26622315
PMCPMC4663735
OpenAlexW2188190150

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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.