Angiogenesis is essential for tumor growth and metastasis. Understanding the regulation of tumor angiogenesis has become increasingly important. MicroRNAs (miRNAs) are small noncoding RNAs that function in diverse biological processes via post-transcriptional regulation. Extensive studies have revealed two important regulatory roles of miRNAs in tumor angiogenesis: miRNAs in tumor cells affect the activity of endothelial cells via non-cell-autonomous mechanisms, and miRNAs in endothelial cells regulate the cell-autonomous behavior. Recent advances have further highlighted the role of tumor-derived extracellular vesicles in the regulation of tumor angiogenesis via transferring miRNAs to endothelial cells. In this review, we summarize the regulatory role of miRNA in tumor angiogenesis, with a highlight on clinical implications of miRNAs as biomarkers for anti-angiogenic therapy response, and as therapeutic interventions against tumor angiogenesis in vivo.

Recent advancements in technology have significantly expanded the scope of tumor research, progressing from the study of individual cells to more intricate tissue and organ-level analyses. Tumor organoids have emerged as a highly realistic platform for investigating tumor growth, development, and their interactions with the surrounding microenvironment. However, a notable limitation of these organoids is their lack of the diverse cellular composition typically observed in actual tumors, which hinders their ability to fully replicate the complexity of the tumor microenvironment. Immune cells play a pivotal role, and tumor immunology has become a major research hotspot. Research in tumor immunology aims to elucidate how the immune system recognizes and attacks tumor cells, as well as how tumor cells evade immune surveillance. In recent years, there has been growing interest in co-culturing immune cells with tumor organoids, an approach that has yielded valuable insights into the intricate interactions between tumors and the immune system. The aim of this paper is to review and discuss the progress achieved in co-culturing tumor organoids with immune cells. By doing so, we hope to offer a new perspective and enhance our understanding of the complexity and diversity inherent in the tumor microenvironment.

Protein lysine methylation is a critical and dynamic post-translational modification that can regulate protein stability and function. This post-translational modification is regulated by lysine methyltransferases and lysine demethylases. Recent studies using mass-spectrometric techniques have revealed that in addition to histones, a great number of transcription factors are also methylated, often at multiple sites and to different degrees (mono-, di-, trimethyl lysine). The biomedical significance of transcription factor methylation in human diseases, including cancer, has been explored recently. Some studies have demonstrated that interfering with transcription factor lysine methylation both in vitro and in vivo can inhibit cancer cell proliferation, thereby reversing tumor progression. The inhibitors targeting lysine methyltransferases and lysine demethylases have been under development for the past two decades, and may be used as potential anticancer agents in the clinic. In this review, we focus on the current findings of transcription factor lysine methylation, and the effects on both transcriptional activity and target gene expression. We outlined the biological significance of transcription factor lysine methylation on tumor progression and highlighted its clinical value in cancer therapy.

Cancer heterogeneity has posed a great challenge to traditional cancer treatment, with the reappearance of cancer heterogeneity of inter and intra patients being especially critical. Based on this, personalized therapy has emerged as significant research focus in recent and even future years. Cancer-related therapeutic models are developing, including cell lines, patient-derived xenografts, organoids, etc. Organoids are three-dimensional in vitro models emerged in the past dozen years and are able to reproduce the cellular and molecular composition of the original tumor. These advantages demonstrate the great potential for patient-derived organoids to develop personalized anticancer therapies, including preclinical drug screening and the prediction of patient treatment response. The impact of microenvironment on cancer treatment cannot be underestimated, and the remodeling of microenvironment also allows organoids to interact with other technologies, among which organs-on-chips is a representative one. This review highlights the use of organoids and organs-on-chips as complementary reference tools in treating colorectal cancer from the perspective of clinical efficacy predictability. We also discuss the limitations of both techniques and how they complement each other well.