Evidence map›Paper›PMID 36614243›Full record

ArticleInternational journal of molecular sciences2023

Claudin-3 Loss of Expression Is a Prognostic Marker in Castration-Resistant Prostate Cancer.

María J Orea, Javier C Angulo, Ana González-Corpas, David Echegaray, Marcos Marvá, María V T Lobo, Begoña Colás, Santiago Ropero

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.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
3.1field-weighted citation impact, top 8% 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, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Claudins in Cancer: A Current and Future Therapeutic Target.International journal of molecular sciences · 2024
    Review
  5. Review
  6. Article
  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 2 institutions in 1 country.

María J OreaDepartamento de Biología de Sistemas, Unidad Docente de Bioquímica y Biología Molecular, Universidad de Alcalá, 28805 Alcalá de Henares, Spain.
Javier C AnguloDepartamento Clínico, Facultad de Ciencias Médicas, Universidad Europea, 28005 Madrid, Spain.ORCID 0000-0002-1735-8792
Ana González-CorpasDepartamento de Biología de Sistemas, Unidad Docente de Bioquímica y Biología Molecular, Universidad de Alcalá, 28805 Alcalá de Henares, Spain.
David EchegarayDepartamento de Biología de Sistemas, Unidad Docente de Bioquímica y Biología Molecular, Universidad de Alcalá, 28805 Alcalá de Henares, Spain.
Marcos MarváDepartamento de Física y Matemáticas, Unidad Docente de Matemáticas, Universidad de Alcalá, 28805 Alcalá de Henares, Spain.ORCID 0000-0003-4703-8615
María V T LoboDepartamento de Ciencias Biomédicas I, Biología Celular y Genética, Universidad de Alcalá, 28805 Alcalá de Henares, Spain.
Begoña ColásDepartamento de Biología de Sistemas, Unidad Docente de Bioquímica y Biología Molecular, Universidad de Alcalá, 28805 Alcalá de Henares, Spain.
Santiago RoperoDepartamento de Biología de Sistemas, Unidad Docente de Bioquímica y Biología Molecular, Universidad de Alcalá, 28805 Alcalá de Henares, Spain.
Universidad de Alcalá · ESHospital Universitario de Getafe · ES

Funding

Instituto de Salud Carlos III PI16/594 and PI19/213
6 · The paper itself

Abstract

Castration-resistant prostate cancer (CRPC) development is the foremost concern after treatment of patients with high risk with locally advanced or metastatic prostate cancer. Androgen receptor (AR) is the main driver of CRPC development, through its interaction with epigenetic modifier genes, placing epigenetics modifications in the forefront of CRPC development. Comparing the DNA methylation and expression profile of androgen-sensitive and -refractory prostate cancer cells, we describe the epigenetic silencing of claudin-3 (CLDN3) in AR positive cells resistant to androgen deprivation (LNCaP-abl). CLDN3 silencing was associated with DNA methylation, loss of histone acetylation and H3K27 methylation, and was re-expressed by the combined treatment with the epigenetic modulators Aza and SAHA. From a functional point of view, CLDN3 loss was associated with increased cellular invasion. Immunohistochemical analysis showed decreased CLDN3 expression in samples from CRPC patients. Interestingly, CLDN3 expression was significantly decreased in samples from patients with high total Gleason score (≥8) and locally advanced tumors. Finally, CLDN3 loss of expression was associated with worse disease-free survival and time to clinical progression. In conclusion, our findings strongly indicate that epigenetic silencing of CLDN3 is a common event in CRPC that could be useful as a molecular marker for the prognosis of prostate cancer patients and to discriminate aggressive from indolent prostate tumors.

Indexed as

Prostatic Neoplasms, Castration-ResistantAndrogen AntagonistsAndrogensCell Line, TumorClaudin-3HumansMalePrognosisReceptors, AndrogenAndrogen AntagonistsAndrogensClaudin-3Receptors, Androgencastration-resistant prostate cancerCLDN3DNA methylationprognosisprostate

Identifiers

PMID36614243
PMCPMC9820886
OpenAlexW4313519528

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.