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M2 type macrophages promote OSCC progress via conferring resistance to Erastin-induced ferroptosis
Chuanchao Su1,2, Zhen Gu1, Jingfei Wang1
1Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Introduction:
M2 type macrophages could promote oral squamous cell carcinoma (OSCC) progress. Ferroptosis is a newly discovered type of programmed cell death and inhibition of ferroptosis in many tumor models could promote tumor progression. This study aims to investigate whether M2 type macrophages could influence the progression of OSCC by regulating the ferroptosis of tumor cells.
Methods:
Immunohistochemical staining was performed to verify the correlation between the expression of CD206 representing M2 type macrophage infiltration in tumor tissue, and GPX4 representing the ability to resist ferroptosis in vivo. In vitro, treat OSCC cells with ferroptosis inducers at different concentrations, detect their effects on ferroptosis, and meanwhile observe their impacts on the proliferation, migration and invasion abilities of OSCC cells; stimulate macrophages to generate different polarization states and identify them. Then, OSCC cells with different levels of ferroptosis were treated with products from macrophages of different polarized states, and the effects on ferroptosis and proliferation, migration and invasion ability of OSCC cells were observed and detected.
Results:
CD206 and GPX4 expression in OSCC clinical samples were positively correlated. With the downregulation of ferroptosis, the proliferation, migration and invasion of OSCC cells were inhibited, and M2 type macrophages can upregulate ferroptosis of OSCC cells, meanwhile enhancing their proliferation, migration and invasion capacity.
Conclusions:
Our studies demonstrated M2 type macrophages could accelerate the progression of OSCC by augmenting the capacity of OSCC cells to resist ferroptosis.
Clinical Significance:
Our studies might offer insights for the application of ferroptosis or macrophage polarization in the therapy of OSCC.
Insights
M2 macrophages accelerate oral squamous cell carcinoma (OSCC) progression by enhancing tumor cell resistance to ferroptosis, a cell death pathway. This suggests targeting ferroptosis or M2 macrophages could be potential therapies for OSCC.
Area of Science:
- Oncology
- Immunology
- Cell Biology
Background:
- M2 macrophages are implicated in promoting oral squamous cell carcinoma (OSCC) progression.
- Ferroptosis, a distinct form of programmed cell death, plays a role in tumor suppression; its inhibition can drive tumor growth.
- Understanding the interplay between M2 macrophages and ferroptosis in OSCC is crucial for therapeutic development.
Purpose of the Study:
- To investigate if M2 macrophages influence OSCC progression by regulating tumor cell ferroptosis.
- To explore the correlation between M2 macrophage infiltration and ferroptosis resistance in OSCC.
- To determine the impact of M2 macrophage-induced ferroptosis modulation on OSCC cell behavior.
Main Methods:
- Immunohistochemistry to assess CD206 (M2 marker) and GPX4 (ferroptosis resistance marker) expression in OSCC tissues.
- In vitro experiments exposing OSCC cells to ferroptosis inducers and analyzing proliferation, migration, and invasion.
- Co-culture systems involving polarized macrophages and OSCC cells to evaluate effects on ferroptosis and cancer cell aggressiveness.
Main Results:
- A positive correlation was observed between CD206 and GPX4 expression in OSCC samples.
- Downregulation of ferroptosis correlated with inhibited OSCC cell proliferation, migration, and invasion.
- M2 macrophages were found to upregulate ferroptosis in OSCC cells, concurrently enhancing their proliferation, migration, and invasion capacity.
Conclusions:
- M2 macrophages accelerate OSCC progression by increasing cancer cell resistance to ferroptosis.
- These findings suggest potential therapeutic strategies targeting ferroptosis or macrophage polarization for OSCC treatment.
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