RESUMEN
Functional gastrointestinal disorders (FGIDs) were highly prevalent and involve gastrointestinal discomfort characterized by non-organic abnormalities in the morphology and physiology of the gastrointestinal tract. According to the Rome IV criteria, irritable bowel syndrome and functional dyspepsia are the most common FGIDs. Complementary and alternative medicines are employed by increasing numbers of individuals around the world, and they include herbal and dietary supplements, acupuncture, and hypnosis. Of these, herbal and dietary supplements seem to have the greatest potential for relieving FGIDs, through multiple modes of action. However, despite the extensive application of natural extracts in alternative treatments for FGIDs, the safety and effectiveness of food and orally ingested food-derived extracts remain uncertain. Many randomized controlled trials have provided compelling evidence supporting their potential, as detailed in this review. The consumption of certain foods (eg, kiwifruit, mentha, ginger, etc) and food ingredients may contribute to the alleviation of symptoms associated with FGID,. However, it is crucial to emphasize that the short-term consumption of these components may not yield satisfactory efficacy. Physicians are advised to share both the benefits and potential risks of these alternative therapies with patients. Furthermore, larger randomized clinical trials with appropriate comparators are imperative.
RESUMEN
Colon cancer is one of the most common types of cancer and more than 80% of colon cancer cases are associated with Wnt-ß-catenin signaling activation. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a multi-functional long non-coding RNA that is overexpressed in many types of cancers, including colon cancer. In this study, MALAT1 and ß-catenin were found to be overexpressed in tumor samples from 62 patients with colon cancer. A positive correlation was identified between MALAT1 levels and ß-catenin protein levels in tumors. MALAT1 was found to upregulate ß-catenin protein levels in HCT116 and LOVO cells without changing the mRNA expression levels. ß-catenin degradation was confirmed to be upregulated in MALAT1-knockdown cells and inhibited in cells overexpressing MALAT1 overexpressing. MALAT1 was then identified as a negative regulator of GSK-3ß; it did so via promotion of H3K27 trimethylation of the promoter region. In conclusion, MALAT1 is an oncogene in colon cancer, which inhibits ß-catenin degradation by upregulating H3K27 trimethylation and repressing GSK-3ß expression.
