Colorectal cancer (CRC) is known as the third most common cancer as well as the fourth most deadly cancer worldwide. CRC accounts for approximately 10 % of all new cancer cases globally, remaining the second most frequent cause of cancer-related deaths. MicroRNAs (miRNAs) are a class of small noncoding RNAs that can affect a variety of cellular and molecular targets. Depending on the cell environment in which the information is expressed, miRNAs can serve as a CRC suppressor or promoter and play essential roles in several biological processes. In this review, we summarized the relationship between miRNAs and proliferation, metastasis, angiogenesis, autophagy, apoptosis, and the chemoradiotherapy of CRC, revealing that relevant miRNAs could serve as potential targets for CRC therapy.

Mammals have several organs comprising various cells with different functions. Furthermore, eukaryotic cells are compartmentalized into functionally distinct organelles. Thus, for good organismal health, exosomes, which play an important role in cell‐to‐cell communication, interact closely with oxidative stress. Oxidative stress, which is recognized as a type of intracellular second signal, is aggravated by reactive species. As a subtype of reactive species, reactive oxygen species (ROS) can be produced on the extracellular face of the plasma membrane by NADPH oxidases, via the mitochondrial electron transport chain, in peroxisomes, and in the lumen of the endoplasmic reticulum. The scavenging of ROS is mainly dependent on peroxiredoxins, including GSH peroxidases, peroxiredoxins 3 and 5, and thioredoxin reductase. Intracellular ROS increase the number of intracellular multivesicular bodies (MVBs) by restraining their degradation in lysosomes, thereby enhancing the release of exosomes under the synergy of the depletion of exofacial GSH, which can be regulated by oxidative stress. In contrast, higher ROS levels can decrease the yield of exosomes by activating cellular autophagy to degrade MVBs. Moreover, exosomes can transfer the characteristics of parent cells to recipient cells. Here, we review the interaction between oxidative stress and exosomes in the hope of providing insights into their interplay.

Tumor-derived exosomes (TDEs) are actively produced and released by tumor cells and carry messages from tumor cells to healthy cells or abnormal cells, and they participate in tumor metastasis. In this review, we explore the underlying mechanism of action of TDEs in tumor metastasis. TDEs transport tumor-derived proteins and non-coding RNA to tumor cells and promote migration. Transport to normal cells, such as vascular endothelial cells and immune cells, promotes angiogenesis, inhibits immune cell activation, and improves chances of tumor implantation. Thus, TDEs contribute to tumor metastasis. We summarize the function of TDEs and their components in tumor metastasis and illuminate shortcomings for advancing research on TDEs in tumor metastasis.

Tumour-derived exosomes (TDEs) are actively produced and released by tumour cells and carry messages from tumour cells to normal or abnormal cells residing at close or distant sites. TDEs participate in every process of tumour metastasis. However, the occurrence and development of tumours depend on the specific functions acquired by tumour cells on the primary and metastatic foci. In this review, we discussed that TDEs regulate the initial mechanism of metastasis, the formation of a pre-metastatic niche, immunosuppression and angiogenesis. In addition, we investigated the signalling pathways and effective components of TDEs and discussed that inhibition of exosomes can inhibit tumour progression. Finally, we discussed the application and future development of TDEs. An understanding of several molecular players and processes involved in metastasis can lead to the development of effective, targeted approaches to prevent metastasis and treat cancer.

Tumor cells actively release large quantities of exosomes, which pivotally participate in the regulation of cancer biology, including head and neck cancer (HNC). Exosome biogenesis and release are complex and elaborate processes that are considered to be similar to the process of exocyst-mediated vesicle delivery. By analyzing the expression of exocyst subunits and their role in patients with HNC, we aimed to identify exocyst and its functions in exosome biogenesis and investigate the molecular mechanisms underlying the regulation of exosome transport in HNC cells. We observed that exocysts were highly expressed in HNC cells and could promote exosome secretion in these cells. In addition, downregulation of exocyst expression inhibited HN4 cell proliferation by reducing exosome secretion. Interestingly, immunofluorescence and electron microscopy revealed the accumulation of multivesicular bodies (MVBs) after the knockdown of exocyst. Autophagy, the major pathway of exosome degradation, is not activated by this intracellular accumulation of MVBs, but these MVBs are consumed when autophagy is activated under the condition of cell starvation. Rab11a, a small GTPase that is involved in MVB fusion, also interacted with the exocyst. These findings suggest that the exocyst can regulate exosome biogenesis and participate in the malignant behavior of tumor cells.

Globally, gastric cancer (GC) is the fifth most common tumor. It is necessary to identify novel molecular subtypes to guide patient selection for specific target therapeutic benefits. Multi-omics data, including transcriptomics RNA-sequencing (mRNA, LncRNA, miRNA), DNA methylation, and gene mutations in the TCGA-STAD cohort were used for the clustering. Ten classical clustering algorithms were executed to recognize patients with different molecular features using the "MOVICS" package in R. The activated signaling pathways were evaluated using the single-sample gene set enrichment analysis. The differential distribution of gene mutations, copy number alterations, and tumor mutation burden was compared, and potential responses to immunotherapy and chemotherapy were also assessed. Two molecular subtypes (CS1 and CS2) were recognized by ten clustering algorithms with consensus ensembles. Patients in the CS1 group had a shorter average overall survival time (28.5 vs. 68.9 months, P = 0.016), and progression-free survival (19.0 vs. 63.9 months, P = 0.008) as compared to those in the CS2 group. Extracellular associated biological process activation was higher in the CS1 group, while the CS2 group displayed the enhanced activation of cell cycle-associated pathways. Significantly higher total mutation numbers and neoantigens were observed in the CS2 group, along with specific mutations in TTN, MUC16, and ARID1A. Higher infiltration of immunocytes was also observed in the CS2 group, reflective of the potential immunotherapeutic benefits. Moreover, the CS2 group could also respond to 5-fluorouracil, cisplatin, and paclitaxel. The similar diversity in clinical outcomes between CS1 and CS2 groups was successfully validated in the external cohorts, GSE62254, GSE26253, GSE15459, and GSE84437. The findings provided novel insights into the GC subtypes through integrative analysis of five -omics data by ten clustering algorithms. These could provide potential clinical therapeutic targets based on the specific molecular features.