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Using 22C3 Anti-PD-L1 Antibody Concentrate on Biopsy and Cytology Samples from Non-small Cell Lung Cancer Patients
Published on: September 25, 2018
The CD300c antibody CL7 suppresses tumor growth by regulating the tumor microenvironment in non-small cell lung
Soyoung Kim1, Ik-Hwan Han1, Suin Lee2
1Department of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Abstract:
Despite advances in therapy, non-small cell lung cancer (NSCLC) continues to rank among the deadliest cancers worldwide. Targeting immunosuppressive components within the tumor microenvironment (TME) has emerged as a promising therapeutic strategy. Unlike M1 tumor-associated macrophages (TAMs), M2-like TAMs contribute to NSCLC progression by promoting an immunosuppressive tumor microenvironment (TME), highlighting the need for tumor microenvironment remodeling. CL7, a monoclonal antibody that targets the activating receptor CD300c on human monocytes and macrophages, was selected as a therapeutic candidate because CD300c engagement triggers MAPK and NF-κB signaling pathways, promoting M1 macrophage polarization and antitumor immune activation. To evaluate the therapeutic potential of CL7, we established an orthotopic NSCLC model by inoculating LLC-luc cells into the left lung of mice. We administered CL7 intraperitoneally at doses of 5 or 10 mg/kg twice a week. Only representative data from the 10 mg/kg CL7 group are shown to maintain consistency with subsequent analyses (flow cytometry, RT-qPCR, and IHC). Tumor growth was significantly suppressed in the CL7-treated group compared to the PBS control group. CL7 treatment also modulated the tumor microenvironment by increasing the population of M1 macrophages and CD8+ T cells, while decreasing the population of regulatory T cells. Our findings suggest that CL7 exerts antitumor effects in NSCLC by reprogramming the immunosuppressive landscape of the TME and enhancing antitumor immunity.
Insights
CL7, a novel antibody, effectively suppresses non-small cell lung cancer (NSCLC) growth by reprogramming the tumor microenvironment (TME). It enhances anti-tumor immunity by promoting M1 macrophages and CD8+ T cells while reducing regulatory T cells.
Area of Science:
- Immunology
- Oncology
- Cancer Research
Background:
- Non-small cell lung cancer (NSCLC) remains a leading cause of cancer mortality globally.
- The tumor microenvironment (TME) plays a critical role in NSCLC progression, with M2-like tumor-associated macrophages (TAMs) promoting immunosuppression.
- Targeting immunosuppressive elements within the TME is a key therapeutic strategy for NSCLC.
Purpose of the Study:
- To evaluate the therapeutic potential of CL7, a monoclonal antibody targeting CD300c, in an orthotopic non-small cell lung cancer model.
- To investigate CL7's effects on tumor growth and the immune landscape within the tumor microenvironment.
- To determine if CL7 can reprogram the immunosuppressive TME and enhance anti-tumor immunity.
Main Methods:
- An orthotopic non-small cell lung cancer (NSCLC) model was established in mice by inoculating LLC-luc cells into the lung.
- CL7 was administered intraperitoneally at 10 mg/kg twice weekly.
- Tumor growth, macrophage polarization (M1/M2), CD8+ T cell infiltration, and regulatory T cell populations were assessed using flow cytometry, RT-qPCR, and immunohistochemistry (IHC).
Main Results:
- CL7 treatment significantly suppressed tumor growth in the orthotopic NSCLC model compared to the PBS control.
- CL7 administration led to an increased population of M1 macrophages and CD8+ T cells within the tumor microenvironment.
- A decrease in the population of regulatory T cells was observed in CL7-treated mice.
Conclusions:
- CL7 demonstrates significant anti-tumor effects in non-small cell lung cancer.
- CL7 exerts its therapeutic effects by reprogramming the immunosuppressive tumor microenvironment.
- CL7 enhances anti-tumor immunity, suggesting its potential as a novel therapeutic agent for NSCLC.
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