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Blocking the FSTL1-DIP2A Axis Improves Anti-tumor Immunity
Chie Kudo-Saito1, Akiko Ishida2, Yuji Shouya2
1Department of Immune Medicine, National Cancer Center Research Institute, Tokyo 104-0045, Japan; Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo 160-8582, Japan.
Cell Reports
|August 16, 2018
Summary
Blocking follistatin-like 1 (FSTL1) significantly suppresses cancer progression by targeting its receptor DIP2A. This approach shows promise for overcoming treatment resistance where immune checkpoint inhibitors have limitations.
Area of Science:
- Oncology
- Immunology
- Cell Biology
Background:
- Immune dysfunction contributes to cancer treatment resistance.
- Current immune checkpoint blockade therapies have limited clinical efficacy.
- Follistatin-like 1 (FSTL1) is implicated in immune dysfunction mediated by mesenchymal stromal/stem cells (MSCs).
Purpose of the Study:
- To investigate the role of FSTL1 in cancer progression and immune evasion.
- To evaluate the therapeutic potential of targeting the FSTL1-DIP2A axis.
- To assess the correlation between FSTL1/DIP2A expression and patient prognosis.
Main Methods:
- Utilized mouse tumor models with increased MSCs.
- Assessed the impact of blocking FSTL1 versus immune checkpoint pathways.
- Examined the role of DIP2A as the FSTL1 receptor.
- Analyzed FSTL1/DIP2A co-expression in non-small cell lung cancer (NSCLC) patient tissues.
Main Results:
- Blocking FSTL1, but not immune checkpoints, suppressed cancer progression and metastasis in preclinical models.
- FSTL1-induced immunoresistance is dependent on DIP2A expression in tumor cells.
- FSTL1/DIP2A co-positivity in NSCLC tissues correlates with poor patient prognosis.
Conclusions:
- The FSTL1-DIP2A axis is a critical mediator of tumor-induced immune resistance.
- Targeting the FSTL1-DIP2A pathway represents a novel strategy to enhance anti-tumor immunity.
- This approach may overcome limitations of current immunotherapies for certain cancers.
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