Loading
Life sciences · Journal article
International Journal of Drug Delivery Technology · November 2, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Colorectal cancer (CRC) remains a leading cause of cancer-related morbidity and mortality worldwide. Emerging evidence implicates muscarinic acetylcholine receptors, particularly the M3 subtype (M3R), in CRC progression. M3R activation by acetylcholine and bile acids stimulates oncogenic signaling cascades, including EGFR transactivation, MAPK/ERK, PI3K/Akt, and matrix metalloproteinase induction. Elevated M3R expression correlates with poor prognosis, underscoring its potential as a biomarker and therapeutic target. Novel ligands— including orthosteric antagonists, allosteric modulators, and biased ligands—offer promising strategies to selectively disrupt tumorigenic signaling. This review synthesizes mechanistic insights, preclinical and clinical evidence, and translational challenges, highlighting future opportunities for M3R-targeted therapies in CRC.