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High incidence of colorectal cancer (CRC) is influenced by diet low in fiber (source of short chain fatty acids, SCFAs, natural agonists for free fatty acid receptor type 2 (FFAR2)) and high in fat (main source of long chain fatty acids, LCFAs, FFAR4 agonists). FFAR2 and FFAR4 are downregulated in CRC. In this study, we characterized whether the anticancer effects of SCFAs and LCFAs are FFAR-dependent in in vitro and in vivo models of CRC. In vitro, SW-480 cell growth was determined after incubation with FFARs ligands (SCFAs: acetate, butyrate; LCFAs: palmitate, stearate) using MTT assay. Cell migration and invasion were investigated by wound healing and transwell-based invasion assays. In vivo, SCFAs and LCFAs were administered to azoxymethane/dextran sodium sulfate-treated mice. Real-time qPCR and Western blot were used to determine FFARs expression. SCFAs and LCFAs significantly decreased SW-480 cell growth, migration and invasion capacities. Combination of SCFAs and LCFAs induced synergistic inhibitory effects on CRC cell growth and motility. FFAR2 and FFAR4 expression were elevated in CRC cells treated with butyrate as well as with butyrate+acetate, and butyrate+palmitate+stearate. Concurrently, only FFAR4 expression was increased in CRC cells incubated with LCFAs. In vivo, treatment with LCFAs, but not SCFAs increased ffar2 and Ffar4 expression. Our findings showed that SCFAs and LCFAs inhibit cancer cell growth and their migration and invasion capabilities. Our study evidenced that the anticancer effects of SCFAs- and LCFAs are mediated by FFAR2 and FFAR4., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Agata Binienda reports financial support was provided by Ministry of Education and Science of the Republic of Poland. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2025. Published by Elsevier B.V.)

Background: Cyclic vomiting syndrome (CVS) is a disorder characterized by sudden, recurrent episodes of severe nausea and vomiting. The pathophysiology of CVS is not known but genetic factors that regulate emetic neurocircuitry have been proposed. The aim of this study was to investigate whether different variations in genes encoding serotonin receptors (HTRs) are associated with susceptibility to CVS and/or CVS symptoms., Methods: This case-control study included 70 patients with CVS:16 male and 54 female, and 2504 healthy controls from the 1000 Genomes Project database. Single-nucleotide polymorphisms (SNPs) in genes encoding serotonin receptors (HTR1B, HTR1D, HTR3B and HTR3C) and correlations between SNPs and the symptoms of CVS were determined., Key Results: Our study discovered that patients with GG, AA and GG genotypes of HTR1B/D rs6296, rs6298 and rs6300, respectively, as well as the CC genotype of HTR3B rs176744 are associated with an increased risk (p < 0.001), whereas allele C in rs3788987 (HTR3B, p < 0.01) and allele A in rs6766410 (HTR3C, p < 0.05) were associated with a decreased risk of CVS. In addition, statistical analysis indicated that CVS patients with GA or AA genotypes of HTR1D rs676643 gene have a seven-fold increase in risk of depression compared to patients with GG genotype (p < 0.01)., Conclusions and Inferences: Our study revealed for the first time that variations in 5-HTR genes may contribute to CVS susceptibility and CVS-related symptoms., (© 2025 John Wiley & Sons Ltd.)