ArticleOncogene2026
Serotonin receptor type 7 (5-HT7) promotes colorectal cancer progression by activating Wnt/β-catenin signaling via interacting with CK1ε.
Article in Oncogene, 2026. 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.
- Plant-Derived Bioactive Compounds in Inflammation-Related Cancers: Mechanisms and Therapeutic Potential.Plants (Basel, Switzerland) · 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
5-hydroxytryptamine (5-HT; serotonin), a well-known neurotransmitter, can promote the development of colorectal cancer (CRC). 5-HT exerts distinct physiological and pathological effects through engagement with specific 5-HT receptors. However, the receptors mediating tumor-promoting effects in CRC remain largely unknown. Here, we found that 5-HT receptor 7 (5-HT7) was significantly upregulated in CRC tumor tissues. Elevated 5-HT7 protein levels correlated positively with tumor burden, pathological grade, and lymph node metastasis, and negatively with overall survival in CRC patients. In CRC cells, lentivirus-mediated 5-HT7 overexpression enhanced proliferation, migration, and invasion, whereas RNA interference-mediated knockdown suppressed these processes. 5-HT (10 μM) increased 5-HT7 expression and had similar tumor-promoting effects in CRC cells, which were suppressed by 5-HT7 knockdown. In nude mice, 5-HT7 overexpression increased tumor size and lung metastasis, while knockdown produced the opposite effects. Mechanistically, 5-HT7 interacted with CK1ε, leading to Dishevelled (Dvl) phosphorylation, β-catenin accumulation, and activation of the Wnt/β-catenin signaling pathway. CK1ε knockdown or treatment with the CK1ε-specific inhibitor PF4800567 blocked 5-HT7-induced Wnt/β-catenin activation and reduced tumor growth and metastasis. Molecular docking and mutagenesis assays identified R13 and R372 in CK1ε and R427 and W472 in 5-HT7 as key residues mediating their interaction. These sites were essential for 5-HT7-driven Wnt/β-catenin activation. Collectively, this study identifies 5-HT7 as a functional receptor promoting CRC progression via Wnt/β-catenin signaling. These findings support the therapeutic potential of targeting 5-HT7 and its interaction with CK1ε in CRC.
Indexed as
Identifiers
41299067What 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.