Tumor microenvironment (TME) is composed of extracellular matrix (ECM), stromal cells, fibroblasts, endothelial cells, and innate and adaptive immune cells around tumor cells. The immune cells and secreted molecules in TME play a vital role in the occurrence, development, metastasis, immunotherapy, and drug resistance of thoracic tumors by interacting with tumor cells.
In this context, the DNA methylation pattern of differentiated cells regulates tissue-specific gene transcription. A considerable amount of DNA methylation has influence in the occurrence and development of tumors by affecting TME. Many studies have found that abnormal methylation of genes can affect the immune infiltration of TME, which is closely related to the prognosis of cancer. For example, a study in 2021 found that DNA methylation of neurofilament medium (NEFM) was significantly negatively correlated with levels of B cells, CD8 + T/ CD4 + T cells, macrophages, neutrophils, and dendritic cells infiltration in breast cancer. DNA methylation of NEFM is also associated with poor prognosis.
Drugs targeting DNA methylation have also become a promising direction for immunotherapy. In addition, DNA methylation works in drug resistance in cancer. For example, ZEB1 induces promoter methylation of estrogen receptor a (ER-a), causing anti-estrogen resistance in breast cancer.
Thoracic tumors are common cancers worldwide and include tumors occurring in the chest cavity, with lung cancer being by far the most common one, but also thymic or tracheal cancers. Exploring potential mechanisms and therapeutic targets of DNA methylation and TME is helpful to deepen the understanding of these diseases and promote the research of potential treatment.
The aim of this research topic is to elucidate the function of DNA methylation and TME in thoracic tumors, including its effects in tumorigenesis, metastasis, immune response, and immunotherapy resistance. We welcome the authors to submit original research and review articles that can help shed new light on DNA methylation, TME, immunotherapy, and drug resistance of thoracic tumors.
(1) The molecular mechanism of interaction between TME and tumor cells in thoracic cancer.
(2) The mechanism of DNA methylation in thoracic tumors
(3) The effect of DNA methylation on the TME of thoracic tumors
(4) DNA methylation, TME, and diagnosis and prognosis of thoracic tumors
(5) Therapies targeting DNA methylation or intercellular interactions in TME
(6) Mechanisms of drug resistance and strategies to overcome immunotherapy resistance
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation are considered out of the scope of this section.
Tumor microenvironment (TME) is composed of extracellular matrix (ECM), stromal cells, fibroblasts, endothelial cells, and innate and adaptive immune cells around tumor cells. The immune cells and secreted molecules in TME play a vital role in the occurrence, development, metastasis, immunotherapy, and drug resistance of thoracic tumors by interacting with tumor cells.
In this context, the DNA methylation pattern of differentiated cells regulates tissue-specific gene transcription. A considerable amount of DNA methylation has influence in the occurrence and development of tumors by affecting TME. Many studies have found that abnormal methylation of genes can affect the immune infiltration of TME, which is closely related to the prognosis of cancer. For example, a study in 2021 found that DNA methylation of neurofilament medium (NEFM) was significantly negatively correlated with levels of B cells, CD8 + T/ CD4 + T cells, macrophages, neutrophils, and dendritic cells infiltration in breast cancer. DNA methylation of NEFM is also associated with poor prognosis.
Drugs targeting DNA methylation have also become a promising direction for immunotherapy. In addition, DNA methylation works in drug resistance in cancer. For example, ZEB1 induces promoter methylation of estrogen receptor a (ER-a), causing anti-estrogen resistance in breast cancer.
Thoracic tumors are common cancers worldwide and include tumors occurring in the chest cavity, with lung cancer being by far the most common one, but also thymic or tracheal cancers. Exploring potential mechanisms and therapeutic targets of DNA methylation and TME is helpful to deepen the understanding of these diseases and promote the research of potential treatment.
The aim of this research topic is to elucidate the function of DNA methylation and TME in thoracic tumors, including its effects in tumorigenesis, metastasis, immune response, and immunotherapy resistance. We welcome the authors to submit original research and review articles that can help shed new light on DNA methylation, TME, immunotherapy, and drug resistance of thoracic tumors.
(1) The molecular mechanism of interaction between TME and tumor cells in thoracic cancer.
(2) The mechanism of DNA methylation in thoracic tumors
(3) The effect of DNA methylation on the TME of thoracic tumors
(4) DNA methylation, TME, and diagnosis and prognosis of thoracic tumors
(5) Therapies targeting DNA methylation or intercellular interactions in TME
(6) Mechanisms of drug resistance and strategies to overcome immunotherapy resistance
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation are considered out of the scope of this section.
