ArticleCancer reports (Hoboken, N.J.)2026
Role of Latrophilin-1 and Latrophilin-2 as Downstream Effectors of Androgen Receptor Signaling in Urothelial Tumorigenesis.
Article in Cancer reports (Hoboken, N.J.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundAccumulating evidence indicates a critical role of androgen receptor (AR) in the pathogenesis of male-dominant urothelial cancer. Meanwhile, the functions of latrophilins (LPHNs), a subfamily of G protein-coupled receptors, remain largely uncharacterized in neoplastic conditions.
aimsTo determine the functional role of LPHN1 and LPHN2 in association with AR signaling in urothelial tumorigenesis. METHODS AND
resultsAR overexpression in immortalized human normal urothelial SVHUC cells or androgen treatment in SVHUC-AR cells markedly increased the expression levels of LPHN1 and LPHN2. Chromatin immunoprecipitation assay demonstrated that AR could bind to the promoter regions of their encoded genes, ADGRL1 and ADGRL2. In SVHUC-AR cells exposed to a chemical carcinogen 3-methylcholanthrene to induce neoplastic transformation, shRNA-mediated knockdown of LPHN1 or LPHN2 significantly reduced their oncogenic activity, as measured by the ability of the resultant cells to form colonies and migrate. Immunohistochemistry in surgical specimens further revealed significantly higher levels of LPHN1 and LPHN2 expression in non-muscle-invasive bladder tumors than in adjacent non-neoplastic urothelial tissues.
conclusionsThe present findings suggest that LPHN1 and LPHN2 function as downstream mediators of AR signaling and promote urothelial tumorigenesis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.