Evidence map›Paper›PMID 33172426›Full record

ArticleBMC cancer2020

B7-H6, an immunoligand for the natural killer cell activating receptor NKp30, reveals inhibitory effects on cell proliferation and migration, but not apoptosis, in cervical cancer derived-cell lines.

Nehla Banu, Annie Riera-Leal, Jesse Haramati, Pablo Cesar Ortiz-Lazareno, Sandeep Surendra Panikar, Blanca Estela Bastidas-Ramirez, Gloria Yareli Gutierrez-Silerio, Fabiola Solorzano-Ibarra, Martha Cecilia Tellez-Bañuelos, Jorge Gutierrez-Franco and 3 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

7 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Enhancing NK cell-mediated tumor killing of B7-H6Molecular therapy. Oncology · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Review
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

13 authors at 5 institutions in 2 countries.

Nehla BanuInstituto de Enfermedades Crónico Degenerativas, Departamento de Biología Molecular y Genómica, CUCS, Universidad de Guadalajara, Sierra Mojada # 950, Colonia Independencia, CP, 44340, Guadalajara, Jalisco, Mexico.
Annie Riera-LealInstitute for Regenerative Cures, Department of Dermatology, University of California-Davis, Davis, USA.
Jesse HaramatiLaboratorio de Inmunobiología, Departamento de Biología Celular y Molecular, CUCBA, Universidad de Guadalajara, Guadalajara, Mexico.
Pablo Cesar Ortiz-LazarenoDivisión de Inmunología, CIBO, Instituto Mexicano del Seguro Social, Guadalajara, Mexico.
Sandeep Surendra PanikarCentro de Física Aplicada y Tecnología Avanzada, Universidad Nacional Autónoma de México, Querétaro, Mexico.
Blanca Estela Bastidas-RamirezInstituto de Enfermedades Crónico Degenerativas, Departamento de Biología Molecular y Genómica, CUCS, Universidad de Guadalajara, Sierra Mojada # 950, Colonia Independencia, CP, 44340, Guadalajara, Jalisco, Mexico.
Gloria Yareli Gutierrez-SilerioInstituto de Enfermedades Crónico Degenerativas, Departamento de Biología Molecular y Genómica, CUCS, Universidad de Guadalajara, Sierra Mojada # 950, Colonia Independencia, CP, 44340, Guadalajara, Jalisco, Mexico.
Fabiola Solorzano-IbarraInstituto de Enfermedades Crónico Degenerativas, Departamento de Biología Molecular y Genómica, CUCS, Universidad de Guadalajara, Sierra Mojada # 950, Colonia Independencia, CP, 44340, Guadalajara, Jalisco, Mexico.
Martha Cecilia Tellez-BañuelosLaboratorio de Inmunobiología, Departamento de Biología Celular y Molecular, CUCBA, Universidad de Guadalajara, Guadalajara, Mexico.
Jorge Gutierrez-FrancoUnidad Académica de Ciencias Químico Biológicas y Farmacéuticas, Universidad Autónoma de Nayarit, Tepic, Mexico.
Miriam Ruth Bueno-TopeteInstituto de Enfermedades Crónico Degenerativas, Departamento de Biología Molecular y Genómica, CUCS, Universidad de Guadalajara, Sierra Mojada # 950, Colonia Independencia, CP, 44340, Guadalajara, Jalisco, Mexico.
Ana Laura Pereira-SuarezLaboratorio de Inmunología, Departamento de Fisiología, CUCS, Universidad de Guadalajara, Guadalajara, Mexico.
Susana Del Toro-ArreolaInstituto de Enfermedades Crónico Degenerativas, Departamento de Biología Molecular y Genómica, CUCS, Universidad de Guadalajara, Sierra Mojada # 950, Colonia Independencia, CP, 44340, Guadalajara, Jalisco, Mexico. susana@cucs.udg.mx.ORCID http://orcid.org/0000-0003-4120-6796
Universidad de Guadalajara · MXCalifornia Institute for Regenerative Medicine · USMexican Social Security Institute · MXUniversidad Autónoma de Nayarit · MXUniversidad Nacional Autónoma de México · MX

Funding

Consejo Nacional de Ciencia y Tecnología (CONACYT) 2017-290195Consejo Nacional de Ciencia y Tecnología (CONACYT) PN-2015-993Universidad de Guadalajara REC/CINV/RG/025/2019
6 · The paper itself

Abstract

backgroundAlthough great progress has been made in treatment regimens, cervical cancer remains as one of the most common cancer in women worldwide. Studies focusing on molecules that regulate carcinogenesis may provide potential therapeutic strategies for cervical cancer. B7-H6, an activating immunoligand expressed by several tumor cells, is known to activate NK cell-mediated cytotoxicity once engaged with its natural receptor NKp30. However, the opposite, that is, the effects in the tumor cell triggered by B7-H6 after interacting with NKp30 has not yet been well explored.

methodsIn this study, we evaluated the surface expression of B7-H6 by flow cytometry. Later, we stimulated B7-H6 positive cervical cancer derived-cell lines (HeLa and SiHa) with recombinant soluble NKp30 (sNKp30) protein and evaluated biological effects using the impedance RTCA system for cell proliferation, the scratch method for cell migration, and flow cytometry for apoptosis. Cellular localization of B7-H6 was determined using confocal microscopy.

resultsNotably, we observed that the addition of sNKp30 to the cervical cancer cell lines decreased tumor cell proliferation and migration rate, but had no effect on apoptosis. We also found that B7-H6 is selectively maintained in tumor cell lines, and that efforts to sort and purify B7-H6 negative or positive cells were futile, as negative cells, when cultured, regained the expression of B7-H6 and B7-H6 positive cells, when sorted and cultivated, lost a percentage of B7-H6 expression.

conclusionsOur results suggest that B7-H6 has an important, as of yet undescribed, role in the biology of the cervical tumor cells themselves, suggesting that this protein might be a promising target for anti-tumor therapy in the future.

Indexed as

ApoptosisCell ProliferationB7 AntigensCell MovementFemaleHumansNatural Cytotoxicity Triggering Receptor 3Tumor Cells, CulturedUterine Cervical NeoplasmsB7 AntigensNatural Cytotoxicity Triggering Receptor 3NCR3LG1 protein, humanNCR3 protein, humanApoptosisB7-H6B7H6Cell migrationCell proliferationCervical cancer

Identifiers

PMID33172426
PMCPMC7654602
OpenAlexW3100273027

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.