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Differences in sensitivity to tumor-specific CTLs between primary and metastatic esophageal cancer cell lines derived
Yoshinobu Ichiki1, Takeshi Hanagiri, Mitsuhiro Takenoyama
1Second Department of Surgery, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan. y-ichiki@med.uoeh-u.ac.jp
Purpose:
MHC antigens and adhesion molecules, such as the intracellular adhesion molecule (ICAM-I), play an important role in cellular immune response. We examined the expression patterns of these molecules in both primary and metastatic esophageal carcinoma cells from the same patient and evaluated the cellular immune responses against these cells.
Materials And Methods:
In the esophageal cancer patient (H122), tumor cell lines were established from primary and subcutaneous metastatic lesions. We compared the expression of cell surface molecules on the metastatic tumor cell line (H122SC) with that on the primary tumor cell line (H122ESO) using flow cytometry. Moreover, we analyzed the differences in cellular immune responses against these cell lines, which expressed similar levels of the Tara antigen, using the Tara antigen-specific CTL clone.
Results:
H122SC ICAM-1 expression was significantly lower in H122ESO, and the Tara antigen-specific CTL clone produced lower levels of TNF in response to H122SC than H122ESO. ICAM-1 transfection into the H122SC rendered these cells as sensitive to the CTL clone as the H122ESO.
Conclusion:
The metastatic tumor cells displayed lower regulated ICAM-1 expression levels and were less sensitive to specific CTLs. ICAM-1 downregulation may be one mechanism by which tumor cells escape immunologic surveillance.
Insights
Metastatic esophageal cancer cells show reduced expression of intercellular adhesion molecule-1 (ICAM-1), making them less susceptible to immune cell attack. Restoring ICAM-1 levels restores immune sensitivity, suggesting a key immune evasion strategy.
Area of Science:
- Oncology
- Immunology
- Cell Biology
Background:
- Major histocompatibility complex (MHC) antigens and adhesion molecules like ICAM-1 are crucial for cellular immune responses.
- Understanding immune evasion mechanisms in metastatic cancer is vital for developing effective therapies.
Purpose of the Study:
- To compare the expression of MHC antigens and adhesion molecules, specifically ICAM-1, between primary and metastatic esophageal carcinoma cells.
- To evaluate the differential cellular immune responses against these primary and metastatic cells.
Main Methods:
- Establishment of primary (H122ESO) and metastatic (H122SC) esophageal tumor cell lines from a single patient.
- Flow cytometry analysis to compare cell surface molecule expression.
- Assessment of T-cell responses using a Tara antigen-specific cytotoxic T lymphocyte (CTL) clone.
Main Results:
- Metastatic H122SC cells exhibited significantly lower ICAM-1 expression compared to primary H122ESO cells.
- The Tara antigen-specific CTL clone produced less tumor necrosis factor (TNF) in response to H122SC cells.
- Restoring ICAM-1 expression in H122SC cells via transfection re-sensitized them to CTL-mediated killing.
Conclusions:
- Downregulation of ICAM-1 in metastatic esophageal cancer cells is associated with reduced sensitivity to specific CTLs.
- Lowered ICAM-1 expression represents a potential mechanism for tumor cells to evade immune surveillance.
- Targeting ICAM-1 could be a therapeutic strategy to enhance anti-tumor immunity.
