Both circular RNAs (circRNAs) and cancer stem cells (CSCs) are separately known to be involved in cancer, but their interaction remains unclear. Here, the regulation of hepatocellular CSC self‐renewal is discovered by a circRNA, circ‐MALAT1, which is produced by back‐splicing of a long noncoding RNA, MALAT1. Circ‐MALAT1 is highly expressed in CSCs from clinical hepatocellular carcinoma samples under the mediation of an RNA‐binding protein, AUF1. Surprisingly, circMALAT1 functions as a brake in ribosomes to retard PAX5 mRNA translation and promote CSCs' self‐renewal by forming an unprecedented ternary complex with both ribosomes and mRNA. The discovered braking mechanism of a circRNA, termed mRNA braking, along with its more traditional role of miRNA sponging, uncovers a dual‐faceted pattern of circRNA‐mediated post‐transcriptional regulation for maintaining a specific cell state.

Small extracellular vesicles (sEVs) such as exosomes are nanoscale membranous particles (<200 nm) that have emerged as crucial targets for liquid biopsy and as promising drug delivery vehicles. They play a significant role in tumor progression as intercellular messengers. They can serve as biomarkers for tumor diagnosis and as drug carriers for cancer treatment. This article reviews recent studies on sEVs in oncology and explores their potential as biomarkers and drug delivery vehicles. Following tumorigenesis, sEVs in the tumor microenvironment (TME) and circulatory system undergo modifications to regulate various events in the TME, including angiogenesis, epithelial-mesenchymal transition (EMT), and tumor immunity, with either pro- or anti-tumor effects. sEVs have been investigated for use as diagnostic and prognostic biomarkers for a variety of tumors, including lung cancer, melanoma, breast cancer, prostate cancer, and hepatocellular carcinoma. sEVs can be used for cancer therapy by packaging drugs or proteins into them through pre- and post-isolation modification techniques. The clinical trials of sEVs as biomarkers and drug carriers are also summarized. Finally, the challenges in the use of sEVs are described and the possible approaches to tackling them are suggested. Overall, sEVs will advance the precision cancer medicine and has shown great potential in clinical applications.

Artificial intelligence (AI)‐driven analysis of comprehensive clinical parameters is bringing about a significant transformation in traditional routine clinical laboratory testing. This transformation impacts the prediction, prevention, diagnosis, and prognosis of human diseases. AI possesses the capability to efficiently analyze and process vast and intricate datasets, thereby facilitating the development of diverse and efficient diagnostic or predictive models. This advancement is fueling significant improvements in laboratory quality, automation, and the accuracy of diagnoses. In this context, we conducted a thorough review and discussion on the progression of AI applications in clinical laboratory medicine, encompassing advancements, implementation, and challenges. Our conclusion underscores that integrating AI into clinical laboratory testing will notably propel personalized precision medicine forward and enhance diagnostic accuracy, especially benefiting patients for whom accurate diagnoses are elusive through traditional laboratory testing systems.

Cancer stem cells (CSCs) are the main cause of tumor development, metastasis, and relapse. CSCs are thus considered promising targets for cancer therapy. However, it is hard to eradicate CSCs due to their inherent plasticity and heterogeneity, and the underlying mechanism of the switch between non‐CSCs and CSCs remains unclear. Here, it is shown that miR‐135a combined with SMYD4 activates Nanog expression and induces the switch of non‐CSCs into CSCs. The miR‐135a level, once elevated, lowers the methylation level of the CG5 site in the Nanog promoter by directly targeting DNMT1. SMYD4 binds to the unmethylated Nanog promoter to activate Nanog expression in Nanog‐negative tumor cells. The in vivo regulation of miR‐135a levels could significantly affect both the CSCs proportion and tumor progression. These findings indicate that DNA methylation of the Nanog promoter modulates the switch of non‐CSCs into CSCs under the control of the miRNA‐135 level. In addition, the related pathways, miR‐135a/DNMT1 and SMYD4, involved in these processes are potential targets for CSC‐targeted therapy.