Evidence map›Paper›PMID 32899449›Full record

ArticleInternational journal of molecular sciences2020

Effects of IGF-1 on Proliferation, Angiogenesis, Tumor Stem Cell Populations and Activation of AKT and Hedgehog Pathways in Oral Squamous Cell Carcinoma.

Jéssica Mariane Ferreira Mendes, Ludmila de Faro Valverde, Manuela Torres Andion Vidal, Bruno Diaz Paredes, Paulo Coelho, Kyan James Allahdadi, Ricardo Della Coletta, Bruno Solano de Freitas Souza, Clarissa Araújo Gurgel Rocha

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 37 citations in OpenAlex.

  1. Effects ofBiology · 2026
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  12. The role of IGF/IGF-1R signaling in the regulation of cancer stem cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
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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

9 authors at 4 institutions in 1 country.

Jéssica Mariane Ferreira MendesGonçalo Moniz Institute, Oswaldo Cruz Foundation (FIOCRUZ), Salvador, Bahia 40296-710, Brazil.
Ludmila de Faro ValverdeGonçalo Moniz Institute, Oswaldo Cruz Foundation (FIOCRUZ), Salvador, Bahia 40296-710, Brazil.
Manuela Torres Andion VidalGonçalo Moniz Institute, Oswaldo Cruz Foundation (FIOCRUZ), Salvador, Bahia 40296-710, Brazil.
Bruno Diaz ParedesCenter for Biotechnology and Cell Therapy, São Rafael Hospital, Salvador, Bahia 41253-190, Brazil.
Paulo CoelhoGonçalo Moniz Institute, Oswaldo Cruz Foundation (FIOCRUZ), Salvador, Bahia 40296-710, Brazil.
Kyan James AllahdadiCenter for Biotechnology and Cell Therapy, São Rafael Hospital, Salvador, Bahia 41253-190, Brazil.
Ricardo Della ColettaDepartment of Oral Diagnosis, School of Dentistry, Campinas State University (UNICAMP), Piracicaba, São Paulo 13414-903, Brazil.
Bruno Solano de Freitas SouzaGonçalo Moniz Institute, Oswaldo Cruz Foundation (FIOCRUZ), Salvador, Bahia 40296-710, Brazil.
Clarissa Araújo Gurgel RochaGonçalo Moniz Institute, Oswaldo Cruz Foundation (FIOCRUZ), Salvador, Bahia 40296-710, Brazil.
Hospital São Rafael · BRFundação Oswaldo Cruz · BRUniversidade Estadual de Campinas (UNICAMP) · BRUniversidade Federal da Bahia · BR

Funding

Fundação de Amparo à Pesquisa do Estado da Bahia APP0006/2016
6 · The paper itself

Abstract

(1) Background: Activation of the PI3K-AKT pathway controls most hallmarks of cancer, and the hedgehog (HH) pathway has been associated with oral squamous cell carcinoma (OSCC) development and progression. We hypothesized that fibroblast-derived insulin-like growth factor-1 (IGF-1) acts in oral squamous cell carcinoma (OSCC) cells, leading to the non-canonical activation of the HH pathway, maintaining AKT activity and promoting tumor aggressiveness. (2) Methods: Primary fibroblasts (MF1) were genetically engineered for IGF-1 overexpression (MF1-IGF1) and CRISPR/Cas9-mediated IGF1R silencing was performed in SCC-4 cells. SCC-4 cells were co-cultured with fibroblasts or incubated with fibroblast conditioned medium (CM) or rIGF-1 for functional assays and the evaluation of AKT and HH pathways. (3) Results: Gene expression analysis confirmed IGF-1 overexpression in MF1-IGF1 and the absence of IGF-1 expression in SCC-4, while elevated IGF1R expression was detected. IGF1R silencing was associated with decreased survival of SCC-4 cells. Ihh was expressed in both MF1 and MF1-IGF1, and increased levels of GLI1 mRNA were observed in SCC-4 after stimulation with CM-MF1. Activation of both PI3K-AKT and the HH pathway (GLI1, Ihh and SMO) were identified in SCC-4 cells cultured in the presence of MF1-IGF1-CM. rIGF-1 promoted tumor cell proliferation, migration, invasion and tumorsphere formation, whereas CM-MF1 significantly stimulated angiogenesis. (4) Conclusions: IGF-1 exerts pro-tumorigenic effects by stimulating SCC-4 cell proliferation, migration, invasion and stemness. AKT and HH pathways were activated by IGF-1 in SCC-4, reinforcing its influence on the regulation of these signaling pathways.

Indexed as

Carcinoma, Squamous CellCell Culture TechniquesCell Line, TumorCell ProliferationHedgehog ProteinsHumansInsulin-Like Growth Factor IMaleMouth NeoplasmsNeoplastic Stem CellsNeovascularization, PathologicPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionSquamous Cell Carcinoma of Head and NeckHedgehog ProteinsIGF1 protein, humanInsulin-Like Growth Factor IPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akthedgehogIGF-1PI3K-AKT

Identifiers

PMID32899449
PMCPMC7555130
OpenAlexW3083706940

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.