ArticleCell death & disease2026
Loss of PRKACB facilitates metastasis of diffuse-type gastric cancer through RhoA signaling activation.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- A risk prediction model for metachronous peritoneal metastasis after radical gastrectomy in gastric cancer based on peripheral blood inflammatory markers and tumor pathological features.American journal of translational research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Diffuse-type gastric cancer (DGC) is characterized by strong invasiveness and poor prognosis, frequently associated with peritoneal metastasis. Dysregulation of protein kinase A catalytic subunit beta (PRKACB) has been implicated in various cancers, but its role in DGC remains unclear. This study investigates the expression, function, and molecular mechanisms of PRKACB in DGC metastasis. PRKACB expression was analyzed by immunohistochemistry in tissue samples from DGC and intestinal-type gastric cancer (IGC) patients. Functional assays and a mouse peritoneal metastasis model were employed to evaluate the impact of PRKACB on metastasis. The interaction between PRKACB and RhoA was explored using co-immunoprecipitation, GST pull-down assays, and in situ proximity ligation assays. PRKACB expression was significantly lower in DGC tissues compared to IGC and adjacent non-tumor tissues. Multivariate Cox regression analysis identified low PRKACB expression as an independent prognostic factor for poor overall survival. In DGC cell lines, PRKACB knockdown enhanced cell migration, invasion, pseudopodia formation, and epithelial-mesenchymal transition (EMT), while PRKACB overexpression suppressed these activities. In vivo experiments demonstrated that PRKACB knockdown promoted earlier onset of peritoneal metastasis. Mechanistically, PRKACB interacted with RhoA and promoted its phosphorylation at S188, thereby inhibiting RhoA signaling and its downstream effectors ROCK1 and FAK. Common RhoA mutations in DGC (V38G and N41K) weakened its interaction with PRKACB, leading to reduced phosphorylation and enhanced metastatic potential. Importantly, RhoA inhibitor treatment reversed the pro-metastatic effects induced by low PRKACB expression. In conclusion, low PRKACB expression promotes DGC metastasis through activation of RhoA signaling, and PRKACB downregulation combined with functional RhoA mutations contributes to the aggressive phenotype of DGC. These findings provide new insights into DGC progression and suggest that PRKACB may serve as both a prognostic biomarker and a potential therapeutic target for DGC patients.
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.