Evidence map›Paper›PMID 36713524›Full record

ArticleFrontiers in oncology2022

Stress induced phosphoprotein 1 overexpression controls proliferation, migration and invasion and is associated with poor survival in oral squamous cell carcinoma.

Mauricio Rocha Dourado, Amr Elseragy, Bruno Cesar da Costa, Fábio Haach Téo, Gustavo Narvaes Guimarães, Renato Assis Machado, Maija Risteli, Wafa Wahbi, Clarissa Araujo Gurgel Rocha, Lívia Máris Ribeiro Paranaíba and 7 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.9field-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

6 citing papers in PubMed, 8 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

17 authors at 10 institutions in 4 countries.

Mauricio Rocha DouradoDepartment of Oral Diagnosis, and Graduate Program in Oral Biology, Piracicaba Dental School, University of Campinas, Piracicaba, São Paulo, Brazil.
Amr ElseragyCancer and Translational Medicine Research Unit, Faculty of Medicine, and Medical Research Center, Oulu University Hospital, University of Oulu, Oulu, Finland.
Bruno Cesar da CostaDepartment of Oral Diagnosis, and Graduate Program in Oral Biology, Piracicaba Dental School, University of Campinas, Piracicaba, São Paulo, Brazil.
Fábio Haach TéoDepartment of Oral Diagnosis, and Graduate Program in Oral Biology, Piracicaba Dental School, University of Campinas, Piracicaba, São Paulo, Brazil.
Gustavo Narvaes GuimarãesDepartment of Biosciences and Graduate Program in Oral Biology, Piracicaba Dental School, University of Campinas, Piracicaba, São Paulo, Brazil.
Renato Assis MachadoDepartment of Oral Diagnosis, and Graduate Program in Oral Biology, Piracicaba Dental School, University of Campinas, Piracicaba, São Paulo, Brazil.
Maija RisteliCancer and Translational Medicine Research Unit, Faculty of Medicine, and Medical Research Center, Oulu University Hospital, University of Oulu, Oulu, Finland.
Wafa WahbiDepartment of Oral and Maxillofacial Diseases, Helsinki University Central Hospital, and Translational Immunology Research Program (TRIMM), University of Helsinki, Helsinki, Finland.
Clarissa Araujo Gurgel RochaGonçalo Moniz Institute, Oswaldo Cruz Foundation, Salvador, Bahia, Brazil.
Lívia Máris Ribeiro ParanaíbaDepartment of Pathology and Parasitology, Institute of Biomedical Sciences, Federal University of Alfenas, Alfenas, Minas Gerais, Brazil.
Wilfredo Alejandro González-ArriagadaFacultad de Odontología, and Centro de Investigación e Innovación Biomédica (CIIB), Universidad de los Andes, Santiago, Chile.
Sabrina Daniela da SilvaLady Davis Institute for Medical Research and Segal Cancer Center, Jewish General Hospital, and Department of Otolaryngology-Head and Neck Surgery, McGill University, Montreal, QC, Canada.
Ana Lucia Carrinho Ayroza RangelDepartment of Oral Pathology and Oral Medicine, Dental School, Western Paranaí State University, Cascavel, Paraná, Brazil.
Marcelo Rocha MarquesDepartment of Biosciences and Graduate Program in Oral Biology, Piracicaba Dental School, University of Campinas, Piracicaba, São Paulo, Brazil.
Carlos Rossa JuniorDepartment of Diagnosis and Surgery, School of Dentistry at Araraquara, São Paulo State University (UNESP), Araraquara, São Paulo, Brazil.
Tuula SaloCancer and Translational Medicine Research Unit, Faculty of Medicine, and Medical Research Center, Oulu University Hospital, University of Oulu, Oulu, Finland.
Ricardo D ColettaDepartment of Oral Diagnosis, and Graduate Program in Oral Biology, Piracicaba Dental School, University of Campinas, Piracicaba, São Paulo, Brazil.
Universidade Estadual de Campinas (UNICAMP) · BRUniversity of Oulu · FICentro Universitário de Araraquara · BRMcGill University · CAUniversidad de Los Andes, Chile · CLUniversidade de São Paulo · BRUniversidade Estadual do Paraná · BRUniversidade Federal da Bahia · BRUniversidade Federal de Alfenas · BRUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Although there have been remarkable achievements in the molecular landscape of oral squamous cell carcinoma (OSCC) in recent years, bringing advances in the understanding of its pathogenesis, development and progression, little has been applied in the prognosis and choosing the optimal treatment. In this study, we explored the influence of the stress induced phosphoprotein 1 (STIP1), which is frequently reported to be highly expressed in many cancers, in OSCCs. Methods: STIP1 expression was assessed in the TCGA database and in two independent cohorts by immunohistochemistry. Knockdown strategy was applied in OSCC cell lines to determine the impact of STIP1 on viability, proliferation, migration and invasion. The zebrafish model was applied for studying tumor formation and metastasis Results: STIP1 was highly expressed in OSCCs and significantly associated with shortened survival and higher risk of recurrence. STIP1 down-regulation decreased proliferation, migration and invasion of tumor cells, and reduced the number of metastases in the Zebrafish model. STIP1 and miR-218-5p were inversely expressed, and the transfection of miR-218-5p mimics into OSCC cells decreased STIP1 levels as well as proliferation, migration and invasion. Conclusion: Our findings show that STIP1 overexpression, which is inversely associated with miR-218-5p levels, contributes to OSCC aggressiveness by controlling proliferation, migration and invasion and is a determinant of poor prognosis.

Indexed as

invasionMIR-218-5poral cancerprognosisproliferationSTIP1

Identifiers

PMID36713524
PMCPMC9874128
OpenAlexW4315498411

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.