Evidence map›Paper›PMID 37175885›Full record

ArticleInternational journal of molecular sciences2023

Endocan Promotes Pro-Tumorigenic Signaling in Lung Cancer Cells: Modulation of Cell Proliferation, Migration and lncRNAs H19 and HULC Expression.

Federica Aliquò, Aurelio Minuti, Angela Avenoso, Giuseppe Mandraffino, Giuseppe Maurizio Campo, Salvatore Campo, Angela D'Ascola, Michele Scuruchi

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 16% 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, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
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

8 authors at 1 institution in 1 country.

Federica AliquòDepartment of Biomedical and Dental Sciences and Morphofunctional Images, University of Messina, Via C. Valeria, 98125 Messina, Italy.
Aurelio MinutiDepartment of Biomedical and Dental Sciences and Morphofunctional Images, University of Messina, Via C. Valeria, 98125 Messina, Italy.
Angela AvenosoDepartment of Biomedical and Dental Sciences and Morphofunctional Images, University of Messina, Via C. Valeria, 98125 Messina, Italy.
Giuseppe MandraffinoDepartment of Clinical and Experimental Medicine, University of Messina, Via C. Valeria, 98125 Messina, Italy.ORCID 0000-0003-0272-2237
Giuseppe Maurizio CampoDepartment of Clinical and Experimental Medicine, University of Messina, Via C. Valeria, 98125 Messina, Italy.
Salvatore CampoDepartment of Biomedical and Dental Sciences and Morphofunctional Images, University of Messina, Via C. Valeria, 98125 Messina, Italy.
Angela D'AscolaDepartment of Clinical and Experimental Medicine, University of Messina, Via C. Valeria, 98125 Messina, Italy.ORCID 0000-0001-7530-1316
Michele ScuruchiDepartment of Clinical and Experimental Medicine, University of Messina, Via C. Valeria, 98125 Messina, Italy.
University of Messina · IT

Funding

University of Messina FFABR_2020
6 · The paper itself

Abstract

Endocan is a circulating proteoglycan secreted by several cell lines and identified as a potential biomarker of inflammation and angiogenesis. Endocan-increased expression has been found in a broad spectrum of human tumors, including lung cancer, and is associated with a poor prognosis. To elucidate the possible mechanism, this study aimed to investigate the role of endocan in non-small-cell lung carcinoma (NSCLC) using an in vitro model of cultured cells. Endocan expression was knocked down by using a specific small interfering RNA. The effects of endocan knockdown have been evaluated on VEGF-A, VEGFR-2, HIF-1α, the long non-coding RNAs H19 and HULC expression, and AKT and ERK 1/2 degree of activation. Cell migration and proliferation have been studied as well. VEGF-A, VEGFR-2, HIF-1α, and the long non-coding RNAs H19 and HULC expression were significantly affected by endocan knockdown. These effects correlated with a reduction of cell migration and proliferation and of AKT and ERK 1/2 activation. Our findings suggest that endocan promotes a more aggressive cancer cell phenotype in NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsRNA, Long NoncodingCell Line, TumorCell MovementCell ProliferationHumansProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2Proto-Oncogene Proteins c-aktRNA, Long NoncodingVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2angiogenesisendocanlong non-coding RNAsNSCLCproteoglycanstumors

Identifiers

PMID37175885
PMCPMC10179037
OpenAlexW4376630037

What OpenQuestion holds

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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.