The Warburg effect in tumor cells involves the uptake of high levels of glucose, enhanced glycolysis, and the metabolism of pyruvate to lactic acid rather than oxidative phos-phorylation to generate energy under aerobic conditions. This effect is closely related to the occurrence, invasion, metastasis, drug resistance, and poor prognosis of gastric cancer (GC). Current research has further demonstrated that the Warburg effect in GC cells is not only mediated by the glycolysis pathway, but also includes roles for mitochondria, noncoding RNAs, and other proteins that do not directly regulate metabolism. As a result, changes in the glycolysis pathway not only lead to abnormal glucose metabolism, but they also affect mitochondrial functions, cellular processes such as apoptosis and cell cycle regulation, and the metabolism of lipids and amino acids. In this review, we discuss metabolic reprogramming in GC based on glycolysis, a possible link between glucose metabolism, lipid metabolism, and amino acid metabolism, and we clarify the role of mitochondria. We also examine recent studies of metabolic inhibitors in GC.

Colorectal cancer (CRC) is the second most common cause of cancer-related death worldwide, and its high rates of relapse and metastasis are associated with a poor prognosis. Despite extensive research, the underlying regulatory mechanisms of CRC remain unclear. Long noncoding RNAs (lncRNAs) are a major type of noncoding RNAs that have received increasing attention in the past few years, and studies have shown that they play a role in many biological processes in CRC. Here, we summarize recent studies on lncRNAs associated with CRC and the signaling pathways and mechanisms underlying this association. We show that dysregulated lncRNAs may be new prognostic and diagnostic biomarkers or therapeutic targets for clinical application. This review contributes not only to our understanding of CRC, but also suggests novel signaling pathways associated with lncRNAs that can be targeted to block or eradicate CRC.

Gastric cancer (GC) is one of the most prevalent and malignant types of cancer worldwide. In China, it is the second most common type of cancer and the malignancy with the highest incidence and mortality rate. Chemotherapy for GC is not always effective due to the development of drug resistance. Drug resistance, which is frequently observed in GC, undermines the success rate of chemotherapy and the survival of patients with GC. The dysregulation of non-coding RNAs (ncRNAs), primarily microRNAs (miRNAs or miRs) and long non-coding RNAs (lncRNAs), is involved in the development of GC drug resistance via numerous mechanisms. These mechanisms contribute to the involvement of a large and complex network of ncRNAs in drug resistance. In this review, we focus on and summarize the latest research on the specific mechanisms of action of miRNAs and lncRNAs that modulate drug resistance in GC. In addition, we discuss future prospects and clinical applications of ncRNAs as potential targeted therapies against the chemoresistance of GC.

Gastric cancer (GC) is the third most common cause of cancer-related death worldwide. Advanced diagnosis and high rates of relapse and metastasis are associated with the poor prognosis of this disease. GC has a complex etiopathogenesis of which the underlying mechanisms remain to be explored. Studies on circular RNAs (circRNAs), noncoding RNAs that may be potential targets in GC, have made substantial progress over the past few years. CircRNAs exert important effects on the onset and progression of GC. Hence, this article aims to summarize the findings of recent studies of circRNAs related to GC and to describe the underlying mechanisms and potential applications. The findings indicate that circRNAs participate in GC regulation, proliferation, invasion, and metastasis through regulating microRNAs, proteins, genes, and signaling pathways. In addition, dysregulated circRNAs may be used as novel diagnostic and prognostic biomarkers or therapeutic targets. This review is expected to facilitate a better understanding of GC, and it suggests novel circRNA-based methods to inhibit or prevent GC.

Cancer is the second leading cause of death worldwide, and no obvious decline in incidence and mortality has occurred in recent years. It is imperative to further investigate the mechanisms underlying tumor progression. Long non-coding RNAs have received considerable attention in recent years because of their major regulatory roles in gene expression. Among them, PVT1 is well-studied, and substantial evidence indicates that PVT1 plays critical roles in the onset and development of cancers. Normally, PVT1 acts as an oncogenic factor by promoting cancer cell proliferation, invasion, metastasis, and drug resistance. Herein, we summarize current knowledge regarding the regulatory effects of PVT1 in cancer progression, as well as the related underlying mechanisms, such as interaction with Myc, modulation of miRNAs, and regulation of gene transcription and protein expression. In extracellular fluid, PVT1 mainly promotes cancer initiation, and it normally enhances cellular cancer characteristics in the cytoplasm and cell nucleus. Regarding clinical applications, its role in drug resistance and its potential use as a diagnostic and prognostic marker have received increasing attention. We hope that this review will contribute to a better understanding of the regulatory role of PVT1 in cancer progression, paving the way for the development of PVT1-based therapeutic approaches in cancer treatment.