Research progress in the cancer field has led to a better understanding of the etiology and pathogenic mechanisms as well as improvement in treatment. However, many cancers undergo relapse and develop resistance to chemotherapy and other treatments. A host of evidence suggests that a small population of cancer cells known as cancer stem cells (CSCs) or stem-like cancer cells, which possess the ability to self-renew and proliferate like normal stem cells, are responsible to maintain cancer stemness. CSCs also appear to show resistance to various anti-cancer therapies and mediate cancer relapse. Because the underlying properties of CSC rely on multiple genes and related signaling pathways, the targeted inhibition of these genes is a promising approach to eliminating cancer stemness.
Cancer stemness plays an important role in the proliferation, metastasis, and relapse of cancer. CSCs were specific cells responsible for cancer stemness. However, the mechanisms underlying the origin of CSCs and their roles in tumorigenesis are not completely understood. Recent studies showed epithelial-mesenchymal transformation (EMT), chronic inflammation, and reprogramming of cell metabolism play important roles in the formation and development of CSC, but what specific genes and cell pathways involved in these processes were not fully known. Thus, in this research topic, we would like to invite studies that describe novel genes which are critical in the origin and development of CSC. We will also encourage authors to clarify the upstream and downstream pathways of these genes and search for the inhibitors of these genes. In addition, recent experimental evidence has substantiated the influence of CSC on the tumor microenvironment. For example, CSCs interact with immune cells including tumor-associated macrophages, myeloid-derived suppressor cells, and T cells. Reciprocally, the cells from the tumor microenvironment also help to sustain CSC stemness and the survival niche for CSCs. We would also encourage studies that explore the relationship between CSC and tumor microenvironment, and analyze the function of specific genes in this process.
This research topic receives articles and reviews on the research of the correlation between cancer stemness and novel genes. The scope includes but is not limited to:
• The reviews summarize the previous findings on the correlation between cancer stemness and genes in EMT, chronic inflammation, cell metabolism reprogramming, and so on.
• Research which identifies new and specific genes or mutations critical for cancer stemness, and elucidates the mechanism of the novel genes or mutations in cancer stemness.
• Research dealing with the relationship between CSC and tumor microenvironment.
• Research dealing with potential therapeutic approaches aimed at specific genes that can exert their action directly in cancer stemness and biologic antibodies or pharmacological activators/inhibitors.
Please note: Manuscripts limited to bioinformatics re-analysis of existing datasets without substantial experimental contribution or detailed representation of novel methodologies will not be considered for publication in this section.
Research progress in the cancer field has led to a better understanding of the etiology and pathogenic mechanisms as well as improvement in treatment. However, many cancers undergo relapse and develop resistance to chemotherapy and other treatments. A host of evidence suggests that a small population of cancer cells known as cancer stem cells (CSCs) or stem-like cancer cells, which possess the ability to self-renew and proliferate like normal stem cells, are responsible to maintain cancer stemness. CSCs also appear to show resistance to various anti-cancer therapies and mediate cancer relapse. Because the underlying properties of CSC rely on multiple genes and related signaling pathways, the targeted inhibition of these genes is a promising approach to eliminating cancer stemness.
Cancer stemness plays an important role in the proliferation, metastasis, and relapse of cancer. CSCs were specific cells responsible for cancer stemness. However, the mechanisms underlying the origin of CSCs and their roles in tumorigenesis are not completely understood. Recent studies showed epithelial-mesenchymal transformation (EMT), chronic inflammation, and reprogramming of cell metabolism play important roles in the formation and development of CSC, but what specific genes and cell pathways involved in these processes were not fully known. Thus, in this research topic, we would like to invite studies that describe novel genes which are critical in the origin and development of CSC. We will also encourage authors to clarify the upstream and downstream pathways of these genes and search for the inhibitors of these genes. In addition, recent experimental evidence has substantiated the influence of CSC on the tumor microenvironment. For example, CSCs interact with immune cells including tumor-associated macrophages, myeloid-derived suppressor cells, and T cells. Reciprocally, the cells from the tumor microenvironment also help to sustain CSC stemness and the survival niche for CSCs. We would also encourage studies that explore the relationship between CSC and tumor microenvironment, and analyze the function of specific genes in this process.
This research topic receives articles and reviews on the research of the correlation between cancer stemness and novel genes. The scope includes but is not limited to:
• The reviews summarize the previous findings on the correlation between cancer stemness and genes in EMT, chronic inflammation, cell metabolism reprogramming, and so on.
• Research which identifies new and specific genes or mutations critical for cancer stemness, and elucidates the mechanism of the novel genes or mutations in cancer stemness.
• Research dealing with the relationship between CSC and tumor microenvironment.
• Research dealing with potential therapeutic approaches aimed at specific genes that can exert their action directly in cancer stemness and biologic antibodies or pharmacological activators/inhibitors.
Please note: Manuscripts limited to bioinformatics re-analysis of existing datasets without substantial experimental contribution or detailed representation of novel methodologies will not be considered for publication in this section.
