ArticleBritish journal of cancer2026
LAMB3 drives gastric cancer progression through SAMD4A-mediated degradation of PHLPP2 mRNA leading to sustained PI3K-Akt activation.
Article in British journal of cancer, 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
13 authors.
Funding
Abstract
backgroundLaminin subunit beta 3 (LAMB3) overexpression has been implicated in cancer progression, but its molecular role in gastric cancer (GC) remains unclear. This study aimed to elucidate how LAMB3 promotes GC malignancy and identify the underlying signalling pathways.
methodsThe clinical significance of LAMB3 was analysed by bioinformatics and immunohistochemistry (IHC) on tissue microarrays. Correlations with clinicopathological parameters were evaluated using Chi-square or Fisher's exact tests, and prognostic value was assessed by log-rank and multivariate Cox regression analyses. Functional assays, including CCK-8, colony formation, Transwell, and xenograft models, were performed to examine the roles of LAMB3 and its downstream effector. Mechanistic studies involved RNA sequencing (RNA-seq), gain- and loss-of-function experiments, RT-qPCR, RNA immunoprecipitation, and western blotting.
resultsLAMB3 was significantly upregulated in GC and correlated with aggressive features and poor prognosis. LAMB3 enhanced GC cell proliferation, migration, and invasion. RNA-seq identified sterile alpha motif domain-containing protein 4 A (SAMD4A) as a critical downstream effector. Silencing SAMD4A suppressed, while its restoration rescued, LAMB3-induced malignancy. Mechanistically, LAMB3 activated PI3K-Akt signalling through SAMD4A-mediated degradation of PHLPP2 mRNA.
conclusionsThis study uncovers a previously unrecognised LAMB3-SAMD4A-PHLPP2 regulatory axis that sustains PI3K-Akt activation and drives GC progression, offering potential prognostic and therapeutic value.
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.