ArticleActa pharmaceutica Sinica. B2026
A novel small molecule inhibitor targeting KHSRP methylation suppresses colon cancer progression.
Article in Acta pharmaceutica Sinica. B, 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RNA-binding proteins (RBPs) are emerging as crucial regulators in cancer, but the development of therapeutic strategies targeting RBPs remains limited. Here, through chemical proteomics approaches, we identify DIQ01 as a novel small-molecule inhibitor of KH-type splicing regulatory protein (KHSRP), an RBP that is aberrantly hyper-expressed in human tumors and plays an essential role in proliferation, metastasis, and tumor progression. DIQ01 specifically binds to the KH3 and KH4 domains (Phe358 as the key residue) of KHSRP, inhibiting its interaction with mRNAs. Furthermore, the binding of DIQ01 diminishes the PRMT5-mediated arginine methylation of KHSRP, a post-translational modification required for its oncogenic activity. Mechanistically, transcriptomic and proteomic profiling suggested that DIQ01 functionally inactivates KHSRP, triggering destabilization and downregulation of its target
Indexed as
Identifiers
What Socratic 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 Socratic graph.