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Patients with EGFR mutation-activated non-small cell lung cancer (NSCLC) are not sensitive to immune checkpoint inhibitor therapy, which is the bottleneck
of lung cancer immunotherapy.
The continuous discovery and elucidating of new mechanisms of tumor immune evasion regulated by tumor microenvironment have brought new hope
to these NSCLC patients.
Recently, the team of Lu Zhimin, Institute of Translational Medicine, Zhejiang University/The First Affiliated Hospital of Zhejiang University School of Medicine, and the team of Academician Hejie of the National Cancer Center/Cancer Hospital of the Chinese Academy of Medical Sciences, conducted a team at Nature Cancer The journal published a research paper in the form of a cover article titled: Silencing EGFR-upregulated expression of CD55 and CD59 activates the complement system and sensitizes lung cancer to checkpoint blockade.
The study revealed that the combination of CD55/CD59 antibodies and PD-1 antibodies can overcome the non-response to immune checkpoint inhibitor therapy in NSCLC patients with EGFR mutations.
The complement system recognizes foreign pathogens and autocells expressing abnormal surface molecules to trigger the release of inflammatory mediators, recruitment of immune cells, phagocytosis, and cell lysis
.
At the same time, the complement system is tightly negatively regulated and inhibited
by membrane-bound complement regulatory proteins (mCRPs, including CD55 and CD59).
Lui and Hatchie's team found that EGFR mutation activation in NSCLC cells increased the expression of CD55 and CD59 in tumor cells, inhibited complement activation and CD8+ T cell activity
.
Further studies found that EGFR mutation activation caused β-catenin to bind to the promoter of the long non-coding RNA LINC00973, thereby inducing LINC00973 expression
.
LINC00973 upregulates the expression of CD55 and CD59 by adsorbing miR-216b and miRNA-150, thereby inhibiting the function of immune cells in the tumor microenvironment mediated by complement activation, and finally achieving tumor immune escape
。 Studies have shown that the combination of CD55/CD59 antibody and PD-1 antibody is more effective in promoting the infiltration of CD8+ T cells and M1 macrophages in tumors, thereby inhibiting tumor growth and significantly prolonging the survival time
of tumor-bearing mice.
EGFR/β-catenin-mediated mechanisms of complement inhibition, immune cell function inhibition, and subsequent promotion of tumor growth
This study revealed the intrinsic regulatory relationship between complement and immune cells in the tumor microenvironment, and provided preclinical evidence that the new strategy of combined blocking mCRP function and PD-1/PD-L1 checkpoint treatment of EGFR mutation activation NSCLC has high clinical translational value
.
Links to papers: style="display: none;">
of lung cancer immunotherapy.
The continuous discovery and elucidating of new mechanisms of tumor immune evasion regulated by tumor microenvironment have brought new hope
to these NSCLC patients.
Recently, the team of Lu Zhimin, Institute of Translational Medicine, Zhejiang University/The First Affiliated Hospital of Zhejiang University School of Medicine, and the team of Academician Hejie of the National Cancer Center/Cancer Hospital of the Chinese Academy of Medical Sciences, conducted a team at Nature Cancer The journal published a research paper in the form of a cover article titled: Silencing EGFR-upregulated expression of CD55 and CD59 activates the complement system and sensitizes lung cancer to checkpoint blockade.
The study revealed that the combination of CD55/CD59 antibodies and PD-1 antibodies can overcome the non-response to immune checkpoint inhibitor therapy in NSCLC patients with EGFR mutations.
The complement system recognizes foreign pathogens and autocells expressing abnormal surface molecules to trigger the release of inflammatory mediators, recruitment of immune cells, phagocytosis, and cell lysis
.
At the same time, the complement system is tightly negatively regulated and inhibited
by membrane-bound complement regulatory proteins (mCRPs, including CD55 and CD59).
Lui and Hatchie's team found that EGFR mutation activation in NSCLC cells increased the expression of CD55 and CD59 in tumor cells, inhibited complement activation and CD8+ T cell activity
.
Further studies found that EGFR mutation activation caused β-catenin to bind to the promoter of the long non-coding RNA LINC00973, thereby inducing LINC00973 expression
.
LINC00973 upregulates the expression of CD55 and CD59 by adsorbing miR-216b and miRNA-150, thereby inhibiting the function of immune cells in the tumor microenvironment mediated by complement activation, and finally achieving tumor immune escape
。 Studies have shown that the combination of CD55/CD59 antibody and PD-1 antibody is more effective in promoting the infiltration of CD8+ T cells and M1 macrophages in tumors, thereby inhibiting tumor growth and significantly prolonging the survival time
of tumor-bearing mice.
EGFR/β-catenin-mediated mechanisms of complement inhibition, immune cell function inhibition, and subsequent promotion of tumor growth
This study revealed the intrinsic regulatory relationship between complement and immune cells in the tumor microenvironment, and provided preclinical evidence that the new strategy of combined blocking mCRP function and PD-1/PD-L1 checkpoint treatment of EGFR mutation activation NSCLC has high clinical translational value
.
Links to papers: style="display: none;">
