ArticlePeerJ2024
Identification of the whole genome of alternative splicing and RNA-binding proteins involved in nintedanib-induced apoptosis in gastric cancer cells.
Article in PeerJ, 2024. 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.
- Unveiling the mysteries of C1QBP in gynecological tumors (Review).Molecular and clinical oncology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: It has been demonstrated that nintedanib can inhibit the proliferation of gastric cancer cells, but the specific mechanism of action is unclear. Objective: Investigating the changes of key factors involved in gene transcription and post-transcriptional regulation during the process of treating gastric cancer with nintedanib. Methods: In this study, we performed transcriptome sequencing on gastric cancer cell groups treated with nintedanib and control groups. The SUVA (Splice sites Usage Variation Analysis) software was used to identify differential alternative splicing (AS) events between the nintedanib-treated group and the control group. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were conducted to assess the functional differences and pathways associated with these events. Finally, a co-expression regulatory network of differentially expressed RNA-binding proteins (RBPs) and differentially spliced genes was established. Results: A total of 915 differential AS events were identified between the two groups, and these differential genes were closely related to the apoptosis pathway. Further analysis revealed that differential RBPs (TAGLN2, TAGLN, SRSF6, PKM, SRSF2, NOC2L, IPO4, C1QBP, DHX9) may affect the anti-proliferative effect of nintedanib on gastric cancer cells by regulating downstream genes involved in cell proliferation and angiogenesis (NR4A1, BBC3, IFI27) through alternative splicing. Conclusion: This study systematically identified important changes in alternative splicing and RNA-binding proteins during the process of nintedanib-induced apoptosis in gastric cancer cells. It innovatively revealed the mechanisms of action of nintedanib in gastric cancer cells and expanded the selection of new targets for gastric cancer treatment.
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.