ArticleCellular oncology (Dordrecht, Netherlands)2025
RAB3A-mediated BAG6 translocation promotes non-small cell lung cancer tumorigenesis and progression.
Article in Cellular oncology (Dordrecht, Netherlands), 2025. 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
11 authors.
Funding
Abstract
purposeRAB3A, a member of the RAS oncogene family, plays a central role in regulated exocytosis and secretion. However, its function, molecular mechanism, and clinical significance in non-small cell lung cancer(NSCLC) remain largely undetermined.
methodsWe analyzed the expression of RAB3A and its correlation with overall survival using multiple databases and immunohistochemistry staining. The oncogenic role of RAB3A in NSCLC was investigated through various cellular assays, including cell viability and colony formation assays. Protein mass spectrometry experiment, immunoprecipitation, immunofluorescence, subcellular fractionation, mitochondria isolation, cycloheximide assays, and lung cancer xenograft mouse models were performed to clarify the molecular mechanism of RAB3A in NSCLC progression.
resultsThe expression of RAB3A was upregulated in NSCLC patients and high level of RAB3A correlated with a poor overall survival. RAB3A depletion inhibited the cell proliferation. Mechanistically, RAB3A knockdown enhanced the nuclear translocation of BAG6-EP300, leading to the acetylation of p53 and Rb. This acetylation strengthened the p53/Rb signaling pathway, thereby suppressing NSCLC progression. Additionally, RAB3A facilitated the transportation of BAG6 to the mitochondria, promoting mitophagy and increasing resistance to cisplatin in NSCLC cells.
conclusionOur findings elucidate the role and underlying mechanisms of RAB3A in NSCLC progression. Thus, RAB3A emerges as a potential prognosis prediction biomarker and therapeutic target for NSCLC patients. CLINICAL TRIAL NUMBER: Not applicable.
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.