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News from April 13, 2021 //---Tumor immunotherapy is currently only able to cause a long-lasting clinical response in some cancer patients.
The treatment tolerance of the remaining patients poses a major challenge to current immunotherapy.
In a recent study, Weiping Zhou's team from the University of Michigan School of Medicine revealed the regulatory effect of stanniocalcin1 protein on tumor immune tolerance, and the relevant results were published in the recent "Cancer Cell" journal.
The treatment tolerance of the remaining patients poses a major challenge to current immunotherapy.
In a recent study, Weiping Zhou's team from the University of Michigan School of Medicine revealed the regulatory effect of stanniocalcin1 protein on tumor immune tolerance, and the relevant results were published in the recent "Cancer Cell" journal.
(Image source: www.
cell.
com)
cell.
com)
As we all know, immune checkpoint-based therapy works to kill cancer cells by activating and enhancing T cell response.
However, most cancer patients do not respond to immune checkpoint therapy.
Therefore, an in-depth understanding of the complex interactions between different immune cell subgroups and tumor cells in the tumor microenvironment is essential for the analysis of the internal and adaptive immune resistance mechanisms, and helps to develop reasonable combination therapies and identify potential new target.
However, most cancer patients do not respond to immune checkpoint therapy.
Therefore, an in-depth understanding of the complex interactions between different immune cell subgroups and tumor cells in the tumor microenvironment is essential for the analysis of the internal and adaptive immune resistance mechanisms, and helps to develop reasonable combination therapies and identify potential new target.
(Figure 1.
There is a correlation between STC1 and immunotherapy tolerance in cancer patients)
There is a correlation between STC1 and immunotherapy tolerance in cancer patients)
Recent studies have shown that genetic and epigenetic mutations in tumors, mutations in IFN-γ and MHC signaling pathways, dysregulation of cytotoxic T cell activity, abnormal metabolic networks, and changes in other biological pathways may all cause tumor cells to appear.
Immunotherapy resistance.
However, these mechanistic studies did not explore the changes in APC-mediated phagocytosis and its impact on immunotherapy resistance.
Immunotherapy resistance.
However, these mechanistic studies did not explore the changes in APC-mediated phagocytosis and its impact on immunotherapy resistance.
(Figure 2, STC1 targets APC to reduce tumor immunogenicity)
In order to explore the immune tolerance mechanism of cancer cells in the tumor microenvironment of patients with clear immune checkpoint treatment responsiveness, the authors analyzed the transcriptome data of melanoma patients who received immune checkpoint treatment, and explored specific unknowns in tumor cells Gene transcription situation.
According to reports, STC1 is a hormone-like protein and is involved in mediating a variety of biological functions.
However, it is still unclear about its receptors and interaction elements, the mechanism of action, and the potential impact of STC1 on tumor immunity.
The results of preclinical models and genetic experiments show that STC1 in tumor cells can affect its response to immunotherapy.
According to reports, STC1 is a hormone-like protein and is involved in mediating a variety of biological functions.
However, it is still unclear about its receptors and interaction elements, the mechanism of action, and the potential impact of STC1 on tumor immunity.
The results of preclinical models and genetic experiments show that STC1 in tumor cells can affect its response to immunotherapy.
On the other hand, antigen-presenting cells (APC) can trigger and activate tumor-associated antigen (TAA)-specific T cell responses, which are critical to the success of immune checkpoint therapy.
The process of antigen presentation depends on whether APCs, including macrophages and dendritic cells (DC), can effectively capture antigens from dead tumor cells through phagocytosis, provide sufficient antigen to T cells and activate T cells.
The authors found that STC1 interacts with CRT in tumor cells, trapping CRT in the mitochondrial area, and reducing the level of CRT in the cell membrane.
Since CRT is the key to "eat me" signal, this process leads to the reduction of APC phagocytosis mediated by cell membrane CRT, resulting in impaired APC antigen presentation and decreased T cell activation.
Therefore, targeting the STC1 protein on the surface of tumor cells can help reduce tumor immune evasion and resistance to immunotherapy.
Based on the above results, the authors believe that STC1 protein acts as a blocker of tumor cell phagocytic signals, and targeting STC1 and its interaction with CRT is a novel anti-cancer immunotherapy method to overcome the resistance of cancer checkpoint therapy.
(Bioon.
com)
The process of antigen presentation depends on whether APCs, including macrophages and dendritic cells (DC), can effectively capture antigens from dead tumor cells through phagocytosis, provide sufficient antigen to T cells and activate T cells.
The authors found that STC1 interacts with CRT in tumor cells, trapping CRT in the mitochondrial area, and reducing the level of CRT in the cell membrane.
Since CRT is the key to "eat me" signal, this process leads to the reduction of APC phagocytosis mediated by cell membrane CRT, resulting in impaired APC antigen presentation and decreased T cell activation.
Therefore, targeting the STC1 protein on the surface of tumor cells can help reduce tumor immune evasion and resistance to immunotherapy.
Based on the above results, the authors believe that STC1 protein acts as a blocker of tumor cell phagocytic signals, and targeting STC1 and its interaction with CRT is a novel anti-cancer immunotherapy method to overcome the resistance of cancer checkpoint therapy.
(Bioon.
com)
Original source: Heng Lin, Ilona Kryczek, Shasha Li et al.
, Stanniocalcin 1 is a phagocytosis checkpoint driving tumor immune resistance.
Cancer Cell (2021).
DOI: https://doi.
org/10.
1016/j.
ccell.
2020.
12.
023
, Stanniocalcin 1 is a phagocytosis checkpoint driving tumor immune resistance.
Cancer Cell (2021).
DOI: https://doi.
org/10.
1016/j.
ccell.
2020.
12.
023
(Figure 1.
There is a correlation between STC1 and immunotherapy tolerance in cancer patients)
There is a correlation between STC1 and immunotherapy tolerance in cancer patients)
Recent studies have shown that genetic and epigenetic mutations in tumors, mutations in IFN-γ and MHC signaling pathways, dysregulation of cytotoxic T cell activity, abnormal metabolic networks, and changes in other biological pathways may all cause tumor cells to appear.
Immunotherapy resistance.
However, these mechanistic studies did not explore the changes in APC-mediated phagocytosis and its impact on immunotherapy resistance.
Immunotherapy resistance.
However, these mechanistic studies did not explore the changes in APC-mediated phagocytosis and its impact on immunotherapy resistance.
(Figure 2, STC1 targets APC to reduce tumor immunogenicity)
In order to explore the immune tolerance mechanism of cancer cells in the tumor microenvironment of patients with clear immune checkpoint treatment responsiveness, the authors analyzed the transcriptome data of melanoma patients who received immune checkpoint treatment, and explored specific unknowns in tumor cells Gene transcription situation.
According to reports, STC1 is a hormone-like protein and is involved in mediating a variety of biological functions.
However, it is still unclear about its receptors and interaction elements, the mechanism of action, and the potential impact of STC1 on tumor immunity.
The results of preclinical models and genetic experiments show that STC1 in tumor cells can affect its response to immunotherapy.
According to reports, STC1 is a hormone-like protein and is involved in mediating a variety of biological functions.
However, it is still unclear about its receptors and interaction elements, the mechanism of action, and the potential impact of STC1 on tumor immunity.
The results of preclinical models and genetic experiments show that STC1 in tumor cells can affect its response to immunotherapy.
On the other hand, antigen-presenting cells (APC) can trigger and activate tumor-associated antigen (TAA)-specific T cell responses, which are critical to the success of immune checkpoint therapy.
The process of antigen presentation depends on whether APCs, including macrophages and dendritic cells (DC), can effectively capture antigens from dead tumor cells through phagocytosis, provide sufficient antigen to T cells and activate T cells.
The authors found that STC1 interacts with CRT in tumor cells, trapping CRT in the mitochondrial area, and reducing the level of CRT in the cell membrane.
Since CRT is the key to "eat me" signal, this process leads to the reduction of APC phagocytosis mediated by cell membrane CRT, resulting in impaired APC antigen presentation and decreased T cell activation.
Therefore, targeting the STC1 protein on the surface of tumor cells can help reduce tumor immune evasion and resistance to immunotherapy.
Based on the above results, the authors believe that STC1 protein acts as a blocker of tumor cell phagocytic signals, and targeting STC1 and its interaction with CRT is a novel anti-cancer immunotherapy method to overcome the resistance of cancer checkpoint therapy.
(Bioon.
com)
The process of antigen presentation depends on whether APCs, including macrophages and dendritic cells (DC), can effectively capture antigens from dead tumor cells through phagocytosis, provide sufficient antigen to T cells and activate T cells.
The authors found that STC1 interacts with CRT in tumor cells, trapping CRT in the mitochondrial area, and reducing the level of CRT in the cell membrane.
Since CRT is the key to "eat me" signal, this process leads to the reduction of APC phagocytosis mediated by cell membrane CRT, resulting in impaired APC antigen presentation and decreased T cell activation.
Therefore, targeting the STC1 protein on the surface of tumor cells can help reduce tumor immune evasion and resistance to immunotherapy.
Based on the above results, the authors believe that STC1 protein acts as a blocker of tumor cell phagocytic signals, and targeting STC1 and its interaction with CRT is a novel anti-cancer immunotherapy method to overcome the resistance of cancer checkpoint therapy.
(Bioon.
com)
Original source: Heng Lin, Ilona Kryczek, Shasha Li et al.
, Stanniocalcin 1 is a phagocytosis checkpoint driving tumor immune resistance.
Cancer Cell (2021).
DOI: https://doi.
org/10.
1016/j.
ccell.
2020.
12.
023
, Stanniocalcin 1 is a phagocytosis checkpoint driving tumor immune resistance.
Cancer Cell (2021).
DOI: https://doi.
org/10.
1016/j.
ccell.
2020.
12.
023
(Figure 2, STC1 targets APC to reduce tumor immunogenicity)
In order to explore the immune tolerance mechanism of cancer cells in the tumor microenvironment of patients with clear immune checkpoint treatment responsiveness, the authors analyzed the transcriptome data of melanoma patients who received immune checkpoint treatment, and explored specific unknowns in tumor cells Gene transcription situation.
According to reports, STC1 is a hormone-like protein and is involved in mediating a variety of biological functions.
However, it is still unclear about its receptors and interaction elements, the mechanism of action, and the potential impact of STC1 on tumor immunity.
The results of preclinical models and genetic experiments show that STC1 in tumor cells can affect its response to immunotherapy.
According to reports, STC1 is a hormone-like protein and is involved in mediating a variety of biological functions.
However, it is still unclear about its receptors and interaction elements, the mechanism of action, and the potential impact of STC1 on tumor immunity.
The results of preclinical models and genetic experiments show that STC1 in tumor cells can affect its response to immunotherapy.
On the other hand, antigen-presenting cells (APC) can trigger and activate tumor-associated antigen (TAA)-specific T cell responses, which are critical to the success of immune checkpoint therapy.
The process of antigen presentation depends on whether APCs, including macrophages and dendritic cells (DC), can effectively capture antigens from dead tumor cells through phagocytosis, provide sufficient antigen to T cells and activate T cells.
The authors found that STC1 interacts with CRT in tumor cells, trapping CRT in the mitochondrial area, and reducing the level of CRT in the cell membrane.
Since CRT is the key to "eat me" signal, this process leads to the reduction of APC phagocytosis mediated by cell membrane CRT, resulting in impaired APC antigen presentation and decreased T cell activation.
Therefore, targeting the STC1 protein on the surface of tumor cells can help reduce tumor immune evasion and resistance to immunotherapy.
Based on the above results, the authors believe that STC1 protein acts as a blocker of tumor cell phagocytic signals, and targeting STC1 and its interaction with CRT is a novel anti-cancer immunotherapy method to overcome the resistance of cancer checkpoint therapy.
(Bioon.
com)
The process of antigen presentation depends on whether APCs, including macrophages and dendritic cells (DC), can effectively capture antigens from dead tumor cells through phagocytosis, provide sufficient antigen to T cells and activate T cells.
The authors found that STC1 interacts with CRT in tumor cells, trapping CRT in the mitochondrial area, and reducing the level of CRT in the cell membrane.
Since CRT is the key to "eat me" signal, this process leads to the reduction of APC phagocytosis mediated by cell membrane CRT, resulting in impaired APC antigen presentation and decreased T cell activation.
Therefore, targeting the STC1 protein on the surface of tumor cells can help reduce tumor immune evasion and resistance to immunotherapy.
Based on the above results, the authors believe that STC1 protein acts as a blocker of tumor cell phagocytic signals, and targeting STC1 and its interaction with CRT is a novel anti-cancer immunotherapy method to overcome the resistance of cancer checkpoint therapy.
(Bioon.
com)
Original source: Heng Lin, Ilona Kryczek, Shasha Li et al.
, Stanniocalcin 1 is a phagocytosis checkpoint driving tumor immune resistance.
Cancer Cell (2021).
DOI: https://doi.
org/10.
1016/j.
ccell.
2020.
12.
023
, Stanniocalcin 1 is a phagocytosis checkpoint driving tumor immune resistance.
Cancer Cell (2021).
DOI: https://doi.
org/10.
1016/j.
ccell.
2020.
12.
023
On the other hand, antigen-presenting cells (APC) can trigger and activate tumor-associated antigen (TAA)-specific T cell responses, which are critical to the success of immune checkpoint therapy.
The process of antigen presentation depends on whether APCs, including macrophages and dendritic cells (DC), can effectively capture antigens from dead tumor cells through phagocytosis, provide sufficient antigen to T cells and activate T cells.
The authors found that STC1 interacts with CRT in tumor cells, trapping CRT in the mitochondrial area, and reducing the level of CRT in the cell membrane.
Since CRT is the key to "eat me" signal, this process leads to the reduction of APC phagocytosis mediated by cell membrane CRT, resulting in impaired APC antigen presentation and decreased T cell activation.
Therefore, targeting the STC1 protein on the surface of tumor cells can help reduce tumor immune evasion and resistance to immunotherapy.
Based on the above results, the authors believe that STC1 protein acts as a blocker of tumor cell phagocytic signals, and targeting STC1 and its interaction with CRT is a novel anti-cancer immunotherapy method to overcome the resistance of cancer checkpoint therapy.
(Bioon.
com)
The process of antigen presentation depends on whether APCs, including macrophages and dendritic cells (DC), can effectively capture antigens from dead tumor cells through phagocytosis, provide sufficient antigen to T cells and activate T cells.
The authors found that STC1 interacts with CRT in tumor cells, trapping CRT in the mitochondrial area, and reducing the level of CRT in the cell membrane.
Since CRT is the key to "eat me" signal, this process leads to the reduction of APC phagocytosis mediated by cell membrane CRT, resulting in impaired APC antigen presentation and decreased T cell activation.
Therefore, targeting the STC1 protein on the surface of tumor cells can help reduce tumor immune evasion and resistance to immunotherapy.
Based on the above results, the authors believe that STC1 protein acts as a blocker of tumor cell phagocytic signals, and targeting STC1 and its interaction with CRT is a novel anti-cancer immunotherapy method to overcome the resistance of cancer checkpoint therapy.
(Bioon.
com)
Original source: Heng Lin, Ilona Kryczek, Shasha Li et al.
, Stanniocalcin 1 is a phagocytosis checkpoint driving tumor immune resistance.
Cancer Cell (2021).
DOI: https://doi.
org/10.
1016/j.
ccell.
2020.
12.
023
, Stanniocalcin 1 is a phagocytosis checkpoint driving tumor immune resistance.
Cancer Cell (2021).
DOI: https://doi.
org/10.
1016/j.
ccell.
2020.
12.
023
Original source: Heng Lin, Ilona Kryczek, Shasha Li et al.
, Stanniocalcin 1 is a phagocytosis checkpoint driving tumor immune resistance.
Cancer Cell (2021).
DOI: https://doi.
org/10.
1016/j.
ccell.
2020.
12.
023
Original source: Stanniocalcin 1 is a phagocytosis checkpoint driving tumor immune resistance. , Stanniocalcin 1 is a phagocytosis checkpoint driving tumor immune resistance.
Cancer Cell (2021).
DOI: https://doi.
org/10.
1016/j.
ccell.
2020.
12.
023
Cancer Cell
