The tumor microenvironment (TME) is a complex biological niche composed of different cell types, and signalling molecules produced by the local and distal cells, including metabolites released from the microbiota. This intricate communication between cancer cells and the surrounding microenvironment can involve mechanisms of local communication over short distances or over large distances via hormones with an effect on crucial cellular processes including cell proliferation, apoptosis, cellular metabolism, genetic instability, angiogenesis, and metastasis promotion. Central and sympathetic nervous system dysfunctions can also influence the TME through multiple mechanisms (i.e. neurogenesis and axonogenesis) thus having a role in cancer pathophysiology. Overall, this complexity is translated in an atlas of signalling networks that are modulated in time and space. It is assumed that modulations at the level of gene and protein expression, protein localization or protein posttranslational modifications account for most of the observed changes in signalling networks that can now be assessed by multi-omics approaches at the single-cell level.
In view of this, it is clear that tumor progression and response to treatment is due to the interplay of these different components and that the combination of therapies targeting different factors is likely to have major clinical efficacy. In this scenario, the role of the microbiota is still not completely investigated and its physiological interaction with the TME should be considered.
The need to find new ways to explore and describe this complexity has prompted this Research Topic, with the aim to bring together novel discoveries that shed light on the molecular pathways and cellular processes involved in TME-cancer crosstalk at the signaling level, and to reveal how these networks can modulate cancer progression and response to treatments.
We specifically welcome Original Research or Review articles that address the following aspects:
- TME-cancer crosstalk, cancer progression and drug resistance
- Cell-cell communication networks in TME
- Cancer signaling networks in TME
- Microbiota signaling in TME
- Noncoding RNA, the TME and microbiota interaction
- Role of the TME and gut microbiome in drug resistance
- Metabolic communication between tumor cells and TME
- Neural regulation of TME
- Organoid models of TME
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Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
The tumor microenvironment (TME) is a complex biological niche composed of different cell types, and signalling molecules produced by the local and distal cells, including metabolites released from the microbiota. This intricate communication between cancer cells and the surrounding microenvironment can involve mechanisms of local communication over short distances or over large distances via hormones with an effect on crucial cellular processes including cell proliferation, apoptosis, cellular metabolism, genetic instability, angiogenesis, and metastasis promotion. Central and sympathetic nervous system dysfunctions can also influence the TME through multiple mechanisms (i.e. neurogenesis and axonogenesis) thus having a role in cancer pathophysiology. Overall, this complexity is translated in an atlas of signalling networks that are modulated in time and space. It is assumed that modulations at the level of gene and protein expression, protein localization or protein posttranslational modifications account for most of the observed changes in signalling networks that can now be assessed by multi-omics approaches at the single-cell level.
In view of this, it is clear that tumor progression and response to treatment is due to the interplay of these different components and that the combination of therapies targeting different factors is likely to have major clinical efficacy. In this scenario, the role of the microbiota is still not completely investigated and its physiological interaction with the TME should be considered.
The need to find new ways to explore and describe this complexity has prompted this Research Topic, with the aim to bring together novel discoveries that shed light on the molecular pathways and cellular processes involved in TME-cancer crosstalk at the signaling level, and to reveal how these networks can modulate cancer progression and response to treatments.
We specifically welcome Original Research or Review articles that address the following aspects:
- TME-cancer crosstalk, cancer progression and drug resistance
- Cell-cell communication networks in TME
- Cancer signaling networks in TME
- Microbiota signaling in TME
- Noncoding RNA, the TME and microbiota interaction
- Role of the TME and gut microbiome in drug resistance
- Metabolic communication between tumor cells and TME
- Neural regulation of TME
- Organoid models of TME
--
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
