ArticleIn vitro cellular & developmental biology. Animal2026
Development of ARL4C antisense oligonucleotide with reduced off-target effects and enhanced efficacy as an anti-cancer drug.
Article in In vitro cellular & developmental biology. Animal, 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ARL4C, a member of the small GTP-binding protein superfamily, is overexpressed in the tumor lesions of various cancers. Antisense oligonucleotide (ASO) therapy targeting ARL4C (ASO-1316-A), a 15-mer ASO, has been shown to inhibit xenograft tumor formation. To enhance therapeutic efficacy and reduce off-target effects, fourteen 18-mer ARL4C-targeting ASOs were developed. Among them, ASO-2025-A/L demonstrated superior suppression of ARL4C mRNA and protein expression compared to ASO-1316-A. In vitro, ASO-2025-A/L inhibited the proliferation, migration, and adhesion abilities of PANC-1 and S2-CP8 pancreatic cancer cells as well as PC-9 lung cancer cells more effectively than ASO-1316-A. ASO-2025-A/L was predicted to reduce the expression of 26 potential off-target genes, compared to 2824 potential off-target genes affected by ASO-1316-A in PANC-1 cells. While ASO-2025-A/L downregulated 317 genes, which were confirmed by RNA-sequence analysis, the majority was involved in cell adhesion pathways downstream of ARL4C signaling, and only two genes corresponded to off-target genes. In vivo, intravenous administration of ASO-2025-A/L inhibited xenograft tumor growth induced by PC-9 and PANC-1 cells, accompanied by a reduction in ARL4C mRNA levels in tumors without elevating serum liver toxicity markers. These findings highlight the development of an improved 18-mer ARL4C-targeting ASO with enhanced therapeutic efficacy and reduced off-target effects.
Indexed as
Identifiers
41792408What 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.