Search

Cancer is a leading cause of death worldwide. Around one-third of the total global cancer incidence and mortality are related to gastrointestinal (GI) cancers. Over the past few years, rapid developments have been made in patient-derived organoid (PDO) models for gastrointestinal cancers. By closely mimicking the molecular properties of their parent tumors in vitro, PDOs have emerged as powerful tools in personalized medicine and drug discovery. Here, we review the current literature on the application of PDOs of common gastrointestinal cancers in the optimization of drug treatment strategies in the clinic and their rising importance in pre-clinical drug development. We discuss the advantages and limitations of gastrointestinal cancer PDOs and outline the microfluidics-based strategies that improve the throughput of PDO models in order to extract the maximal benefits in the personalized medicine and drug discovery process.

N6-methyladenosine (m6A) modification of messenger RNA (mRNA) influences the stability and translation of the transcripts into functional proteins. Recent studies reveal the role of m6A modifications in regulating the metabolism of basic biomolecules such as glucose, lipids and amino acids. Such mechanisms are not only important for physiological functions of normal cells but also prove to be pivotal for the pathogenesis of cancers by driving dysregulated metabolism. M6A writers, readers and erasers function co-operatively to promote aberrant glucose, lipid and amino acid metabolism in cancer cells, which in turn support increased proliferative and metastatic potential. Better understanding of the relationship between m6A and metabolism in malignancy may unravel novel therapeutic targets as well as biomarkers in cancer. In this review, we summarize the recent evidence demonstrating the interplay between m6A modification and cancer metabolism and their therapeutic implications.

Colorectal cancer (CRC) is one of the leading cancers that cause cancer-related deaths worldwide. The gut microbiota has been proved to show relevance with colorectal tumorigenesis through microbial metabolites. By decomposing various dietary residues in the intestinal tract, gut microbiota harvest energy and produce a variety of metabolites to affect the host physiology. However, some of these metabolites are oncogenic factors for CRC. With the advent of metabolomics technology, studies profiling microbiota-derived metabolites have greatly accelerated the progress in our understanding of the host-microbiota metabolism interactions in CRC. In this review, we briefly summarize the present metabolomics techniques in microbial metabolites researches and the mechanisms of microbial metabolites in CRC pathogenesis, furthermore, we discuss the potential clinical applications of microbial metabolites in cancer diagnosis and treatment.