Evidence map›Paper›PMID 33433063›Full record

ArticleMolecular oncology2021

LncRNA SOX2-OT regulates AKT/ERK and SOX2/GLI-1 expression, hinders therapy, and worsens clinical prognosis in malignant lung diseases.

Abril Marcela Herrera-Solorio, Irlanda Peralta-Arrieta, Leonel Armas López, Nallely Hernández-Cigala, Criselda Mendoza Milla, Blanca Ortiz Quintero, Rodrigo Catalán Cárdenas, Priscila Pineda Villegas, Evelyn Rodríguez Villanueva, Cynthia G Trejo Iriarte and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 45 citations in OpenAlex.

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  20. [SOX2-OT/SOX2 axis regulates lung cancer H520 cell migrationNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
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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

13 authors at 2 institutions in 1 country.

Abril Marcela Herrera-SolorioBiomedicine Research Unit (UBIMED), Lung Diseases and Cancer Epigenomics Laboratory, Facultad de Estudios Superiores (FES) Iztacala, National Autonomous University of Mexico (UNAM), Tlalnepantla de Baz, Mexico.ORCID 0000-0001-5292-115X
Irlanda Peralta-ArrietaBiomedicine Research Unit (UBIMED), Lung Diseases and Cancer Epigenomics Laboratory, Facultad de Estudios Superiores (FES) Iztacala, National Autonomous University of Mexico (UNAM), Tlalnepantla de Baz, Mexico.ORCID 0000-0002-6256-9054
Leonel Armas LópezBiomedicine Research Unit (UBIMED), Lung Diseases and Cancer Epigenomics Laboratory, Facultad de Estudios Superiores (FES) Iztacala, National Autonomous University of Mexico (UNAM), Tlalnepantla de Baz, Mexico.ORCID 0000-0001-9490-4294
Nallely Hernández-CigalaBiomedicine Research Unit (UBIMED), Lung Diseases and Cancer Epigenomics Laboratory, Facultad de Estudios Superiores (FES) Iztacala, National Autonomous University of Mexico (UNAM), Tlalnepantla de Baz, Mexico.ORCID 0000-0002-9605-8367
Criselda Mendoza MillaNational Institute of Respiratory Diseases (INER), Ismael Cosío Villegas, Mexico City, Mexico.ORCID 0000-0003-0304-2313
Blanca Ortiz QuinteroNational Institute of Respiratory Diseases (INER), Ismael Cosío Villegas, Mexico City, Mexico.ORCID 0000-0001-6298-0073
Rodrigo Catalán CárdenasThoracic Oncology Unit, Laboratory of Personalized Medicine, Instituto Nacional de Cancerología (INCAN), Mexico City, Mexico.ORCID 0000-0002-4492-813X
Priscila Pineda VillegasBiomedicine Research Unit (UBIMED), Lung Diseases and Cancer Epigenomics Laboratory, Facultad de Estudios Superiores (FES) Iztacala, National Autonomous University of Mexico (UNAM), Tlalnepantla de Baz, Mexico.ORCID 0000-0001-7085-1773
Evelyn Rodríguez VillanuevaGrupo de Investigación en Células Troncales e Ingeniería de Tejidos (GICTIT), Laboratorio de Investigación en Odontología Almaraz, FES-Iztacala, National Autonomous University of México (UNAM), Tlalnepantla de Baz, Mexico.ORCID 0000-0002-6980-108X
Cynthia G Trejo IriarteGrupo de Investigación en Células Troncales e Ingeniería de Tejidos (GICTIT), Laboratorio de Investigación en Odontología Almaraz, FES-Iztacala, National Autonomous University of México (UNAM), Tlalnepantla de Baz, Mexico.ORCID 0000-0002-3423-5217
Joaquín ZúñigaNational Institute of Respiratory Diseases (INER), Ismael Cosío Villegas, Mexico City, Mexico.ORCID 0000-0002-7143-0281
Oscar ArrietaThoracic Oncology Unit, Laboratory of Personalized Medicine, Instituto Nacional de Cancerología (INCAN), Mexico City, Mexico.ORCID 0000-0002-1164-3779
Federico Ávila-MorenoBiomedicine Research Unit (UBIMED), Lung Diseases and Cancer Epigenomics Laboratory, Facultad de Estudios Superiores (FES) Iztacala, National Autonomous University of Mexico (UNAM), Tlalnepantla de Baz, Mexico.ORCID 0000-0002-0252-7899
Autonomous University of Tlaxcala · MXInstituto Nacional de Cancerología · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The involvement of LncRNA SOX2-overlapping transcript (SOX2-OT), SOX2, and GLI-1 transcription factors in cancer has been well documented. Nonetheless, it is still unknown whether co-expressed SOX2-OT/SOX2 or SOX2-OT/SOX2/GLI-1 axes are epigenetically/transcriptionally involved in terms of resistance to oncology therapy and in poorer clinical outcomes for patients with lung cancer. We evaluated the role of SOX2-OT/SOX2 and SOX2-OT/SOX2/GLI-1 axes using RT-qPCR, western blot, immunofluorescence analyses, gene silencing, cellular cytotoxic, and ChIP-qPCR assays on human cell lines, solid lung malignant tumors, and normal lung tissue. We detected that the SOX2-OT/SOX2/GLI-1 axis promotes resistance to tyrosine kinase inhibitor (TKI)-erlotinib and cisplatin-based therapy. Evidence from this study show that SOX2-OT modulates the expression/activation of EGFR-pathway members AKT/ERK. Further, both SOX2-OT and GLI-1 genes are epigenetically regulated at their promoter sequences, in an LncRNA SOX2-OT-dependent manner, mainly through modifying the enrichment of the activation histone mark H3K4me3/H3K27Ac, versus the repressive histone mark H3K9me3/H3K27me3. In addition, we identified that inhibition of SOX2-OT and reduced expression of SOX2/GLI-1 sensitizes lung cancer cells to EGFR/TKI-erlotinib or cisplatin-based treatment. Finally, we show that high co-expression of SOX2-OT/SOX2 transcripts and SOX2/GLI-1 proteins appears to correlate with a poor clinical prognosis and lung malignant phenotype. Collectively, these results present evidence that LncRNA SOX2-OT modulates an orchestrated resistance mechanism, promoting poor prognosis and human lung malignancy through genetic, epigenetic, and post-translational mechanisms.

Indexed as

Cell Line, TumorCisplatinDrug Resistance, NeoplasmEpigenesis, GeneticErlotinib HydrochlorideExtracellular Signal-Regulated MAP KinasesHistonesHumansLung NeoplasmsPrognosisProto-Oncogene Proteins c-aktRNA, Long NoncodingSOXB1 Transcription FactorsZinc Finger Protein GLI1CisplatinErlotinib HydrochlorideExtracellular Signal-Regulated MAP KinasesGLI1 protein, humanHistonesProto-Oncogene Proteins c-aktRNA, Long NoncodingSOX2 protein, humanSOXB1 Transcription FactorsZinc Finger Protein GLI1drug resistanceGLI-1LncRNAlung adenocarcinomaSOX2SOX2-OT

Identifiers

PMID33433063
PMCPMC8024737
OpenAlexW3110649133

What OpenQuestion holds

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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.