Tumor drug resistance is an important issue in cancer treatment, which can affect treatment efficacy and patient survival rate. Recent studies have shown that tumor drug resistance is related to genomic epigenetic regulation. Genomic epigenetic regulation refers to the regulation of gene expression that does not involve changes in DNA sequence, including DNA methylation, histone modification, ubiquitination, and non-coding RNA. These regulatory mechanisms can affect gene expression and function, thereby influencing tumor growth, metastasis, and drug resistance. Tumor drug resistance is associated with DNA methylation. DNA methylation is an important type of genomic epigenetic modification that can suppress gene expression by methylation in the promoter region of genes. In drug resistance, the promoter region of some key genes may be methylated, which reduces their expression and leads to drug resistance. In addition, histone modification can also affect tumor drug resistance. Histone modification is a type of epigenetic modification that adds chemical groups to histones, which can affect gene expression and function. Some studies have shown that the pattern of histone modification in tumor cells may change in drug resistance, which leads to changes in the expression of key genes and affects tumor drug resistance.
Recent research has also found that ubiquitination can also participate in tumor drug resistance. Ubiquitination is an important cellular protein degradation mechanism that can regulate protein stability, location, interaction, and function. Tumor cells can enhance their drug resistance by regulating ubiquitination. For example, ubiquitin ligases can regulate the expression and function of key genes in tumor cells, affecting the growth and metastasis of tumor cells. In addition, some studies have suggested that tumor cells can change their metabolism and energy status by regulating their ubiquitination, thereby enhancing drug resistance. On the other hand, tumor cells can also use ubiquitination to avoid attacks from the immune system. For example, tumor cells can avoid attacks from immune cells by inhibiting specific ubiquitin ligases, thereby enhancing their drug resistance. Additionally, in tumor drug resistance, some non-coding RNAs may also participate in regulating the expression and function of key genes, thereby affecting tumor drug resistance.
Overall, genomic epigenetic regulation can affect tumor growth, metastasis, and drug resistance. Future studies are needed to deeply explore the relationship between genomic epigenetic regulation and tumor drug resistance to provide more effective strategies for tumor treatment and prevention. Among our research topics, original research and review articles are welcome, but not limited to the following topics:
• Exploration of Tumor Drug Resistance Mechanisms from the Epigenetic Perspective: Analysis of the genome and transcriptome data of tumor cells to explore the regulatory role of epigenetic mechanisms on gene expression, as well as their role in tumor drug resistance.
• Analysis of Genome Epigenetic Regulation and Drug Metabolism: Analysis of the metabolic and genomic data of tumor cells to study the role of drug-metabolizing enzymes and transporters in tumor drug resistance.
• The Role of Genome Epigenetic Regulation in Tumor Immune Escape: Study of the effect of epigenetic mechanisms on tumor immune escape, such as antigen expression, T-cell activation, and immune cell infiltration.
Tumor drug resistance is an important issue in cancer treatment, which can affect treatment efficacy and patient survival rate. Recent studies have shown that tumor drug resistance is related to genomic epigenetic regulation. Genomic epigenetic regulation refers to the regulation of gene expression that does not involve changes in DNA sequence, including DNA methylation, histone modification, ubiquitination, and non-coding RNA. These regulatory mechanisms can affect gene expression and function, thereby influencing tumor growth, metastasis, and drug resistance. Tumor drug resistance is associated with DNA methylation. DNA methylation is an important type of genomic epigenetic modification that can suppress gene expression by methylation in the promoter region of genes. In drug resistance, the promoter region of some key genes may be methylated, which reduces their expression and leads to drug resistance. In addition, histone modification can also affect tumor drug resistance. Histone modification is a type of epigenetic modification that adds chemical groups to histones, which can affect gene expression and function. Some studies have shown that the pattern of histone modification in tumor cells may change in drug resistance, which leads to changes in the expression of key genes and affects tumor drug resistance.
Recent research has also found that ubiquitination can also participate in tumor drug resistance. Ubiquitination is an important cellular protein degradation mechanism that can regulate protein stability, location, interaction, and function. Tumor cells can enhance their drug resistance by regulating ubiquitination. For example, ubiquitin ligases can regulate the expression and function of key genes in tumor cells, affecting the growth and metastasis of tumor cells. In addition, some studies have suggested that tumor cells can change their metabolism and energy status by regulating their ubiquitination, thereby enhancing drug resistance. On the other hand, tumor cells can also use ubiquitination to avoid attacks from the immune system. For example, tumor cells can avoid attacks from immune cells by inhibiting specific ubiquitin ligases, thereby enhancing their drug resistance. Additionally, in tumor drug resistance, some non-coding RNAs may also participate in regulating the expression and function of key genes, thereby affecting tumor drug resistance.
Overall, genomic epigenetic regulation can affect tumor growth, metastasis, and drug resistance. Future studies are needed to deeply explore the relationship between genomic epigenetic regulation and tumor drug resistance to provide more effective strategies for tumor treatment and prevention. Among our research topics, original research and review articles are welcome, but not limited to the following topics:
• Exploration of Tumor Drug Resistance Mechanisms from the Epigenetic Perspective: Analysis of the genome and transcriptome data of tumor cells to explore the regulatory role of epigenetic mechanisms on gene expression, as well as their role in tumor drug resistance.
• Analysis of Genome Epigenetic Regulation and Drug Metabolism: Analysis of the metabolic and genomic data of tumor cells to study the role of drug-metabolizing enzymes and transporters in tumor drug resistance.
• The Role of Genome Epigenetic Regulation in Tumor Immune Escape: Study of the effect of epigenetic mechanisms on tumor immune escape, such as antigen expression, T-cell activation, and immune cell infiltration.
